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        <title>Acta Biochimica Polonica | New and Recent Articles</title>
        <link>https://www.frontierspartnerships.org/journals/acta-biochimica-polonica</link>
        <description>RSS Feed for Acta Biochimica Polonica | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-20T12:01:34.155+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15484</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15484</link>
        <title><![CDATA[Genetic architecture of obesity and advances in precision pharmacotherapy: a comprehensive review]]></title>
        <pubdate>2026-04-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Floren Kavaja</author><author>Thomas Liehr</author><author>Gazmend Temaj</author>
        <description><![CDATA[Obesity, a global health catastrophe, arises from complex interactions between environmental factors and genetic predispositions. This review summarizes the current state of knowledge on the genetic basis of obesity and contrasts rare monogenic forms caused by mutations in a single gene with common polygenic forms caused by hundreds of genetic variants with small effects. We highlight important genes in neuroendocrine signaling pathways, particularly the leptin-melanocortin system involving MC4R, LEP, and POMC, as well as newly identified loci from genome-wide association studies such as FTO and SEC16B. The interplay between genetic probability and environmental factors underscores the heterogeneity of obesity phenotypes. Recent advances in pharmacotherapy, such as GLP-1 receptor agonists and dual/triple incretin agonists, demonstrate strong efficacy across various genetic backgrounds and underscore the translational relevance of genetic insights. New findings from different groups support the use of polygenic risk scores to identify individuals at risk and suggest prevention strategies. This review discusses the genomic data on clinical practice and emphasizes the possibilities and challenges of precision medicine in obesity treatment. Future research should focus on length of genetic screening and elucidating gene-environment interactions to optimize treatment outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15939</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15939</link>
        <title><![CDATA[Species barriers in AAV tropism: mechanisms, models, and emerging solutions for clinical translation]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Xinyuan Xu</author>
        <description><![CDATA[Adeno-associated virus (AAV) vectors have become central to in vivo gene therapy across genetic and acquired diseases. Yet despite extensive preclinical validation, AAV programs often encounter translational gaps when advancing from rodents to non-human primates (NHPs) and ultimately to humans. These species barriers arise from differences in capsid–receptor interactions, intracellular trafficking, immune landscapes, and tissue microanatomy. Even within species, strain-level genetic variation can markedly alter vector performance, exemplified by the LY6A-dependent central nervous system (CNS) tropism of AAV-PhP.B in C57BL/6J mice. Old world monkeys, which are evolutionarily closer to humans than new world species, remain the most widely used models for systemic and CNS delivery, yet discrepancies in seroprevalence, complement activity, endothelial biology, and neuronal susceptibility still limit predictability. Recent advances, including machine learning–guided capsid design, deep mutational scanning, and human-derived organoids and explant models, offer powerful tools to bridge these barriers. This mini-review synthesizes current understanding of AAV species barriers and outlines strategies that enhance the robustness and human relevance of AAV gene therapy development.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.16188</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.16188</link>
        <title><![CDATA[Association between systemic inflammatory markers and recurrence risk in benign paroxysmal positional vertigo: a retrospective cohort study]]></title>
        <pubdate>2026-03-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bekir Doğan</author><author>Deniz Baklacı</author>
        <description><![CDATA[ObjectiveBenign paroxysmal positional vertigo (BPPV) is a common vestibular disorder that responds well to canalith repositioning maneuvers but is frequently complicated by recurrence. Increasing evidence suggests that systemic inflammation may influence disease course and recurrence risk. This study aimed to investigate the association between routinely available systemic inflammatory markers and BPPV recurrence within 6 months.MethodsIn this single-center retrospective cohort study, 300 adult patients diagnosed with BPPV between January 2020 and December 2024 were included. Neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), and C-reactive protein (CRP) levels measured at initial presentation were analyzed. Recurrence within 6 months following successful canalith repositioning maneuvers was defined as the primary outcome. Group comparisons were performed using non-parametric tests. Independent predictors of recurrence were identified using multivariable logistic regression analysis, and receiver operating characteristic (ROC) analysis was used to evaluate discriminatory performance.ResultsDuring the six-month follow-up period, recurrence occurred in 78 patients (26.0%). Patients with recurrence had significantly higher NLR and CRP levels compared with those without recurrence (both p < 0.001). SII values were also elevated in the recurrence group, although the difference was less pronounced (p = 0.048). In multivariable analysis adjusted for age, sex, and canal involvement, both NLR (odds ratio [OR]: 1.42; 95% confidence interval [CI]: 1.18–1.71) and CRP (OR: 1.27; 95% CI: 1.10–1.46) emerged as independent predictors of BPPV recurrence. ROC analysis demonstrated moderate discriminatory ability for NLR (AUC = 0.71) and CRP (AUC = 0.69), whereas SII showed limited predictive performance (AUC = 0.62).ConclusionSystemic inflammatory markers, particularly NLR and CRP, are independently associated with recurrence risk in BPPV. Given their low cost and widespread availability, these markers may provide complementary information for early risk stratification. Further prospective and multicenter studies are required to clarify causal mechanisms and confirm clinical applicability.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.16199</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.16199</link>
        <title><![CDATA[Differential in vitro and in vivo responses of Akkermansia muciniphila to Odontosoria biflora (Kaulf.) C.Chr. [Lindsaeaceae] hexane extract in diet- and alloxan-induced BALB/c mice]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Marvie Hamel Darbandi</author><author>Leslie Michelle M. Dalmacio</author>
        <description><![CDATA[Akkermansia muciniphila is a mucin-degrading gut bacterium linked to metabolic health, yet culture-based growth stimulation may not translate to sustained enrichment in vivo. Odontosoria biflora (“tubho”) is traditionally consumed in the Philippines as a herbal tea, but its extract-level activity toward A. muciniphila remains poorly characterized. O. biflora was sequentially extracted (hexane, ethyl acetate, methanol, aqueous) and screened for growth-supporting activity toward A. muciniphila in modified BHI under anaerobic conditions. The most active fraction (hexane; OBE HEX) was evaluated for acute oral tolerability in BALB/c mice according to OECD Tesy No. 423 (up to 2000 mg/kg) and subsequently assessed in a high-fat/high-sugar diet plus alloxan-induced diabetic model. Fecal A. muciniphila-specific qPCR signal was monitored at weeks 0, 1, 2, and 4 using a modified 2−ΔΔCt approach with external ATCC genomic DNA as a reference. OBE-HEX produced the strongest in vitro growth-supporting effect (56.43% at 250 mg/L, p < 0.05; 85.62% at 500 mg/L, p < 0.001) and showed no observable toxicity in vivo. In contrast, in vivo analysis revealed only transient changes in fecal A. muciniphila detection following OBE-HEX administration, whereas sustained elevation was observed only in metformin-treated mice. Untargeted UPLC-ESI-QTOF-MS analysis of OBE-HEX yielded putative identification of 2-O-rhamnosylvitexin and 7-methoxy-9,10-dihydrophenanthrene-2,5-diol. Overall, these findings demonstrate that while O. biflora hexane extract exhibits direct growth-supporting activity toward A. muciniphila in vitro and is orally tolerable, such effects do not translate into sustained in vivo enrichment under diabetic conditions, underscoring the limitations of extrapolating culture-based microbiota screening results to host-associated systems.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15861</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15861</link>
        <title><![CDATA[Structural potential of the 5′ noncoding regions of the mRNAs encoding p53 isoforms]]></title>
        <pubdate>2026-02-19T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Mariola Dutkiewicz</author><author>Paulina Zydowicz-Machtel</author>
        <description><![CDATA[Famous for its nickname “guardian of the genome,” the p53 protein acts, among other things, as a transcription factor in the form of a tetramer, which may consist of different types of p53 isoforms. They differ in length and content of specific domains that are responsible for their functions. The way this factor acts, sometimes opposite to what we would expect from the main protein isoform, depends on which isoforms form the tetramer. There are over a dozen isoforms of the human p53 protein encoded by a single gene, thanks to the use of different transcriptional promoters (DNA level), alternative splicing (pre-mRNA level), and different translation initiation sites (mRNA level). In vitro studies have demonstrated that the use of different translation initiation sites on full-length p53FL mRNA is possible due to specific RNA structures, and that these structures are also responsible for the rate and efficiency of target protein isoform formation. This affects the proportions between the different p53 isoforms present in the cell at a given moment and, consequently, the further fate of the cell. This paper summarizes the knowledge about the importance of the RNA structure (I-III order) of individual p53 transcripts for the fate of the cell and the organism.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15244</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15244</link>
        <title><![CDATA[Bibliometric analysis of research trends on the epiretinal membrane since 2000]]></title>
        <pubdate>2026-02-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>ShuHan Zeng</author><author>Rui Wang</author><author>Jie Chen</author><author>Yue He</author>
        <description><![CDATA[Epiretinal membrane (ERM) is an important retinal disorder, yet its global research landscape has not been systematically evaluated. This study conducted a comprehensive bibliometric analysis of ERM-related publications indexed in the Web of Science Core Collection. Data were analyzed using CiteSpace, bibliometrix, VOSviewer, and the bibliometrix R package to assess publication trends, international collaboration, influential journals, and evolving research topics. A total of 1,059 articles published between 2000 and 2024 were included. The annual number of publications showed a steady increase, with the United States and other developed countries contributing the majority of research output. Journal analysis identified Retina-The Journal of Retinal and Vitreous Diseases as the leading outlet in terms of productivity. Keyword co-occurrence and co-citation analyses revealed that current research hotspots involve epidemiology, molecular mechanisms, imaging biomarkers associated with surgical outcomes, and the emerging use of artificial intelligence in diagnosis and prognosis prediction. These findings provide an integrated overview of ERM research development, highlight major thematic shifts, and offer valuable guidance for future investigations in this field.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15740</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15740</link>
        <title><![CDATA[Advances in endothelial cell targeting by AAV vectors]]></title>
        <pubdate>2026-02-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Milena Cichon</author><author>Alicja Jozkowicz</author><author>Anna Grochot-Przeczek</author>
        <description><![CDATA[Adeno-associated virus (AAV) vectors have become a cornerstone of in vivo gene delivery. However, although the endothelium is the first cellular interface encountered after systemic delivery, native AAV serotypes exhibit poor endothelial transduction, favoring hepatocytes, muscle cells and, neurons instead. This limitation represents a major barrier to gene therapies targeting cardiovascular, neurovascular, and inflammatory diseases. This review summarizes recent advances in redirecting AAV tropism toward endothelial cells (ECs) through genetic capsid engineering, peptide display, and non-genetic surface modification. We highlight the previously underrecognized endothelial tropism of the AAV4 serotype, attributed to its unique recognition of O-linked sialic acids. We also describe multiple approaches to capsid retargeting, including the incorporation of EC-binding peptides that enable cell entry into specific vascular beds, as well as genetic engineering strategies that reduce heparan sulfate proteoglycan (HSPG) binding and hepatocyte transduction while enhancing intracellular trafficking in ECs. In addition, we discuss polymer-coating approaches that allow receptor-specific targeting of ECs with reduced recognition by immune cells. Together, these strategies represent promising avenues for enhancing vascular tropism and transduction efficiency of modified AAVs, moving the field closer to precise vascular gene therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15808</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15808</link>
        <title><![CDATA[Low calcium intake from diet and supplements in a group of Polish patients with SLE – an additional risk for osteoporotic fractures?]]></title>
        <pubdate>2026-02-04T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Jolanta Anna Dardzińska</author><author>Natalia Matysiak</author><author>Karolina Kułakowska</author><author>Marta Jaskólska</author><author>Sylwia Małgorzewicz</author><author>Alessio Molfino</author>
        <description><![CDATA[BackgroundPatients with systemic lupus erythematosus (SLE) are at increased risk of osteoporosis. Despite this, the awareness of adequate dietary calcium intake and other prevention strategies is often underrecognized in clinical practice and guidelines.MethodsDietary calcium intake was assessed using the ADOS-Ca questionnaire, validated for the Polish population, in SLE patients recruited both in person and online from various outpatient clinics. Data on vitamin D supplementation, awareness of osteoporosis risk, and preventive actions initiated by healthcare providers were also collected.ResultsMedian dietary calcium intake was 540 mg/day, below the recommended ≥1,000 mg or ≥1,200 mg (depending on age and sex). Only 25% of patients met these recommendations, including the subgroup of chronically taking glucocorticoids. Calcium supplementation was used by 31% of respondents on long-term glucocorticoid therapy. Regular vitamin D supplementation was reported by 79% of participants. Calcium and vitamin D intake and supplementation did not differ between patients treated and untreated with glucocorticoids. While 57% were aware of their elevated osteoporosis risk, only 32% had received guidance on preventive measures.ConclusionGreater attention to osteoporosis prevention is needed among SLE patients, both from healthcare professionals and the patients themselves. The first and most fundamental step is optimizing calcium intake through diet and supplementation, which is particularly important in undergoing long-term glucocorticoid therapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15388</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15388</link>
        <title><![CDATA[Vitamin D, calcium, phosphates, and magnesium serum level and bone mineral density in patients with type 1 diabetes]]></title>
        <pubdate>2026-02-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Agnieszka Zawada</author><author>Michał Michalak</author><author>Dariusz Naskręt</author><author>Agata Grzelka–Woźniak</author><author>Alicja Ewa Ratajczak-Pawłowska</author><author>Anna Maria Rychter</author><author>Kinga Skoracka</author><author>Aleksandra Szymczak-Tomczak</author><author>Dorota Zozulińska-Ziółkiewicz</author><author>Agnieszka Dobrowolska</author><author>Iwona Krela-Kaźmierczak</author>
        <description><![CDATA[IntroductionAbnormal glucose metabolism, which is a common condition in patients with type 1 diabetes (T1DM), triggers a number of changes in various organs. Additionally, elevated blood glucose level also affects the bones. Bone mineral density (BMD), vitamin D, calcium, phosphates, and magnesium serum concentrations are significant factors assessed in bone metabolism. In this study, we evaluated these factors and the impact of vitamin D supplementation on vitamin D and BMD levels in T1DM patients.Materials and methodsThe study included 66 adults with T1DM and a control group of 66 healthy adults of the same age and weight. Densitometric measurements of the lumbar spine (L1–L4) and femoral neck (FN) were performed using dual-energy X-ray absorptiometry. The concentration of vitamin D, calcium, phosphates, and magnesium in the blood was assessed. All patients completed a questionnaire regarding vitamin D supplementation and symptoms associated with osteoporosis.ResultsSignificant differences in the range, BMD, Z-score and T-score for FN and L1-L4 were observed in diabetic and non-diabetic subjects. Only 50% of participants with diabetes and osteopenia and only 40% of diabetic patients without osteopenia showed optimal vitamin D concentration. There were no differences in BMD, T-score and Z-score of FN, as well as in L1-L4 between the subjects who supplemented and those who did not supplement vitamin D.ConclusionPatients with T1DM are more at risk of developing osteoporosis than healthy individuals. Vitamin D may not be the only factor affecting BMD. Patients with T1DM should be screened for osteoporosis and other complications. Patients with type 1 diabetes should receive higher doses of vitamin D than healthy adults and control their calcium, magnesium and phosphates serum concentrations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15936</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2026.15936</link>
        <title><![CDATA[The role of serum tryptase in COVID-19 pathogenesis and its value as a prognostic marker: a single-center prospective cohort study]]></title>
        <pubdate>2026-01-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alan Majeranowski</author><author>Damian Palus</author><author>Michał Hoffmann</author><author>Zbigniew Heleniak</author><author>Tomasz Stefaniak</author><author>Krzysztof Kuziemski</author>
        <description><![CDATA[BackgroundDysregulated inflammation is central to COVID-19 pathogenesis. Mast cells (MCs) and their protease tryptase are implicated in tissue injury and vascular dysfunction, but the prognostic value of circulating tryptase in COVID-19 remains uncertain.MethodsWe conducted a prospective cohort study including 82 patients with laboratory-confirmed COVID-19 admitted between January and March 2021. On admission, serum tryptase, C-reactive protein (CRP), procalcitonin (PCT), lactate dehydrogenase (LDH), and lymphocyte counts were measured. The objective of this study was to assess whether serum tryptase levels measured upon hospital admission are associated with COVID-19 severity and in-hospital mortality. Statistical analyses comprised t-tests, Mann–Whitney U tests, χ2 tests, receiver operating characteristic (ROC) curve analysis, and logistic regression.ResultsSerum tryptase levels at admission did not differ significantly between patients requiring oxygen and those who did not (mean 5.45 vs. 4.97 μg/L; p = 0.2906) or between survivors and non-survivors (mean 5.24 vs. 5.60 μg/L; p = 0.6486). ROC analysis confirmed limited prognostic performance for tryptase regarding oxygen requirement (AUC = 0.580; p = 0.2972) and mortality (AUC = 0.538; p = 0.6103). By contrast, CRP, PCT, and LDH correlated strongly with disease severity. Elevated PCT (p = 0.0016) and LDH (p = 0.0360) were significantly associated with mortality. Logistic regression showed no independent association between tryptase and adverse outcomes.ConclusionIn this prospective cohort, serum tryptase measured at admission was not associated with COVID-19 severity or mortality, suggesting limited utility as a prognostic biomarker. Established markers, particularly PCT and LDH, outperformed tryptase in predicting adverse clinical outcomes. The negative findings are clinically relevant as they demonstrate that tryptase does not contribute to prognostic risk stratification in COVID-19, and its measurement does not provide added value beyond standard inflammatory biomarkers.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15819</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15819</link>
        <title><![CDATA[RNA splicing in bone diseases: mechanisms, pathogenesis and therapeutics]]></title>
        <pubdate>2026-01-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Linlin Zheng</author><author>Hui Sun</author><author>Ning Li</author><author>Lianqing Wang</author><author>Tianchu Li</author><author>Qiaoli Zhai</author>
        <description><![CDATA[RNA splicing is a fundamental post-transcriptional mechanism that enables the generation of diverse mRNA isoforms from a single gene, thereby expanding proteomic complexity and regulating cell fate decisions. Emerging evidence highlights that dysregulated splicing contributes to the onset and progression of various bone-related diseases, including osteoporosis, osteoarthritis, and skeletal malignancies. In this review, we summarize current knowledge on the core mechanisms of pre-mRNA splicing, with emphasis on alternative splicing events that modulate bone cell differentiation, matrix formation, and tissue homeostasis. We further discuss how aberrant splicing impacts signaling pathways involved in bone metabolism and disease pathogenesis, and we explore the epigenetic and RNA-binding protein networks that fine-tune these processes. Finally, we examine the therapeutic potential of targeting splicing machinery or correcting mis-splicing events using small molecules, antisense oligonucleotides, and RNA-based approaches. This comprehensive overview provides mechanistic insights and highlights splicing regulation as a promising avenue for the diagnosis and treatment of skeletal disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15459</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15459</link>
        <title><![CDATA[Prevalence of vitamin D deficiency and related factors among adults in Tokat province, Türkiye: a community-based cross-sectional study]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Muzaffer Katar</author><author>Rıza Çıtıl</author><author>Yalçın Önder</author><author>Osman Demir</author>
        <description><![CDATA[BackgroundVitamin D deficiency is a major public health concern, worldwide yet data on the adult population in Türkiye remain limited. This study aimed to determine the prevalence of vitamin D deficiency and its associated risk factors in Tokat Province, Türkiye.MethodsA population based cross-sectional study was conducted among 2,225 adults aged ≥20 years through multistage stratified cluster sampling from both urban and rural areas. Data were obtained via structured questionnaires, anthropometric measurements, and fasting blood samples. Serum 25-hydroxyvitamin D3 [25(OH)D3] levels were measured and categorized as deficient (<10 ng/mL), insufficient (10–20 ng/mL), or sufficient (>20 ng/mL). Multivariate logistic regression was used to identify predictors of deficiency.ResultsThe mean age was 47.2 ± 15.2 years, and 54.8% were women. Vitamin D deficiency was present in 38.7% and insufficiency in 46.4% of participants. Deficiency was significantly more common among women, the older adult, obese individuals, and those with lower education levels and chronic diseases (p < 0.05). In the adjusted model female sex (aOR 0.19, 95% CI 0.14–0.27), obesity (aOR 1.76, 95% CI 1.36–2.28), and lower education were independent predictors of deficiency.ConclusionVitamin D deficiency and insufficiency are highly prevalent among adults in Tokat Province, despite adequate sunlight exposure in the region. Public health strategies/interventions should focus on high-risk groups, prioritize particularly women, older adults, and obese individuals through screening, education, and targeted supplementation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15546</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15546</link>
        <title><![CDATA[Hemoglobin as an oxygen gasoreceptor]]></title>
        <pubdate>2025-12-17T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Savani Anbalagan</author>
        <description><![CDATA[In most vertebrates, hemoglobin’s primary function is to transport oxygen and carbon dioxide. Hemoglobin is also expressed in cells such as dopaminergic neurons and chondrocytes, as well as in organelles such as mitochondria. Depending on its location, hemoglobin subunits can interact with proteins involved in various functions, including anion exchange, nitric oxide synthesis, and ATP synthesis. These interactions suggest that hemoglobin has diverse regulatory roles beyond gas transport. During hypoxia and an excess of nitrite and protons, deoxygenated hemoglobin exhibits nitrite reductase activity and produces nitric oxide, a gaseous signaling molecule. Hemoglobin-derived nitric oxide is associated with vasodilation in mammals and the inhibition of mitochondrial respiration in cell cultures. This raises the question of whether hemoglobin functions as a gasoreceptor in these cells or organelles. The HIF1α/PHD2 pathway in mammals and cysteine oxidases in plants are largely responsible for sensing hypoxia, but the identity of oxygen gasoreceptors analogous to the mammalian nitric oxide gasoreceptor soluble guanylate cyclase and the plant ethylene gasoreceptor kinases remains unknown. Since the heme-based dual oxygen-binding and catalytic domain emerged earlier than the allosteric regions, I propose hemoglobin as an oxygen proto-gasoreceptor derivative. Furthermore, since hemoglobin interacts with and regulates proteins depending on its oxygen binding state, I propose that hemoglobin functions as an oxygen gasoreceptor in split-component signal transduction systems. Recognizing hemoglobin as a gasoreceptor will expand the emerging field of gasocrinology to encompass gases that were previously considered primarily metabolic substrates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15550</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15550</link>
        <title><![CDATA[The Dual Edge of zinc: linking excessive intake to obesity, diabetes, hypertension, and cardiovascular risks]]></title>
        <pubdate>2025-12-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Tanushree Das</author><author>Rhea Ahongshangbam</author><author>Romoka Chabungbam</author><author>Kshetrimayum Birla Singh</author>
        <description><![CDATA[Zinc, an essential trace element, plays a pivotal role in numerous physiological processes, including antioxidant defense, immune regulation, and metabolic homeostasis. However, excessive Zn supplementation disrupts these pathways, contributing to the pathogenesis of chronic conditions such as obesity, diabetes mellitus, hypertension, and cardiovascular diseases. This systematic review explores the dual-edged nature of Zn by examining its molecular impacts, including antioxidant enzyme dysregulation, leptin receptor resistance, and inflammatory marker modulation. While optimal Zn levels confer protective benefits, such as improved insulin sensitivity and reduced oxidative stress, excessive intake triggers systemic inflammation, oxidative damage, and metabolic dysregulation. Contrasting evidence highlights dose-dependent effects and variability based on genetic and environmental factors, underscoring the need for tailored dietary guidelines. Knowledge gaps persist regarding Zn toxicity thresholds, long-term impacts, and interactions with other nutrients. Public health policies must prioritize balanced supplementation strategies to mitigate risks while leveraging Zn’s therapeutic potential in chronic disease prevention. This review emphasizes the importance of precision nutrition and evidence-based approaches to optimize Zn’s benefits while minimizing its adverse effects.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15465</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15465</link>
        <title><![CDATA[Gasocrine hypothesis – a potential supplement to cell theory]]></title>
        <pubdate>2025-12-10T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Savani Anbalagan</author>
        <description><![CDATA[Biology textbooks lack precise terms to describe oxygen-based inter-organismal signaling between oxygen-producing and aerobic organisms. To address this gap, I recently proposed the concept of gasocrine signaling, which encompasses all signaling mediated by gaseous molecules and gasoreceptors within and between cells, organisms, and even abiotic factors. Given the fundamental importance of gaseous molecules for life, I propose the gasocrine hypothesis: all cells require gasocrine signaling. This hypothesis can be divided into three sub-hypotheses: First, all living organisms composed of one or more cells require gasocrine signaling to sense, communicate, grow, and propagate. Second, gasocrine signaling mediated via gasoreceptor proteins (or yet to be identified gas-sensing riboceptors) is the most essential cellular and inter-organismal signaling. Third, acellular entities arising from or replicating in pre-existing cells require gasocrine signaling. I propose several potential experiments to falsify these hypotheses. If they withstand falsification, the gasocrine hypothesis would supplement cell theory. It would also provide a novel framework for understanding fundamental biological principles, cellular and organismal communication, and the role of abiotic factors. Furthermore, it establishes the foundation for the emerging field of gasocrinology, which is critical in the context of a changing environment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15672</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15672</link>
        <title><![CDATA[Effects of low concentrations of fatty acids on Escherichia coli depend on the kind of culture medium and incubation temperature]]></title>
        <pubdate>2025-11-17T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Barbara Stencel</author><author>Monika Zielenkiewicz</author><author>Łukasz Grabowski</author>
        <description><![CDATA[Fatty acids play important, yet different roles in bacterial physiology, specifically their growth, either stimulating or inhibiting this parameter which are of biotechnological importance. Here, we present results showing to what degree short- and medium-chain fatty acids (butyric acid (butanoic acid, C4:0); caproic acid (hexanoic acid, C6:0); caprylic acid (octanoic acid, C8:0)), used at relatively low concentrations (in a range of μg/mL, contrary to previously reported mg/mL which revealed inhibitory effects on bacterial growth) affect growth of Escherichia coli K-12 (MG1655 laboratory strain) depending on various conditions. In rich medium (LB) positive effects of all tested fatty acids on E. coli growth were observed, while temperature of incubation (growth at 25 °C and 37 °C was assessed) modulated these effects. In contrast, a slight but significant growth inhibition by fatty acids was observed in a minimal medium (M9) supplemented with glucose. Nonetheless, in minimal medium containing acetate, the effects of these compounds varied, being either positive or negative depending on their concentrations. No measurable bacterial growth was observed in the case of the presence of any tested fatty acids when primary carbon source (glucose or acetate) was removed from a minimal medium before addition of butyric acid, caproic acid or caprylic acid. Our results indicated that effects of low concentrations of fatty acids on E. coli cells depend on growth conditions of bacterial cultures. This may be of biotechnological importance, especially for modulating E. coli growth by using different compositions of media and incubation temperatures.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15218</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15218</link>
        <title><![CDATA[New analogs of 5-substituted-2(1H)-pyridone containing of natural amino acids as potential drugs in idiopathic pulmonary fibrosis. Investigation in silico and preliminary in vitro]]></title>
        <pubdate>2025-11-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Krystyna Dzierzbicka</author><author>Maria Skrzypkowska</author><author>Monika Gensicka-Kowalewska</author><author>Mateusz Daśko</author><author>Bartosz Słomiński</author>
        <description><![CDATA[The aim of our work was to analyze new functionalized analogues of 5-substituted-2(1H)-pyridone containing of natural amino acids derivatives as a potential drugs in idiopathic pulmonary fibrosis (IPF). The creation of connections with natural amino acids was aimed at obtaining anti-fibrotic compounds with better water solubility, increased hydrophilicity, lower toxicity and better pharmacokinetic properties. For the docking studies the corresponding grid box parameters were used: PARPγ, ALK5 andp38. During our initial research we have synthesized and performed biological in vitro studies for two analogues selected on the basis of molecular modeling: 6b and 6f. MTT test have been performed to select concentrations of PFD derivatives for subsequent analysis. We have analyzed HLA-DR and CXCR4 expression on fibroblasts and 24 h migration of TGF-β1-stimulated fibroblasts. We have also explored proliferation and production of TGF-β1 as well as IL-17 by CD3/CD28 beads-stimulated PBMCs. Preliminary studies show that the designed compounds exhibit promising potential as anti-fibrotic therapeutics. Therefore, their activity is worth further exploring.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15744</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.15744</link>
        <title><![CDATA[Editorial: Acta Biochimica Polonica reviews | 2023–2024]]></title>
        <pubdate>2025-11-07T00:00:00Z</pubdate>
        <category>Special Issue Editorial</category>
        <author>Michał Rurek</author><author>Jarosław Czyż</author><author>Zbigniew Heleniak</author><author>Paulina Niedźwiedzka-Rystwej</author><author>Witold N. Nowak</author><author>Milena Paw</author><author>Dawid Wnuk</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.14410</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.14410</link>
        <title><![CDATA[Salivary biomarkers in cancer detection and management]]></title>
        <pubdate>2025-10-20T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Aneeq Munsif</author><author>Alicja Nowaczyk</author><author>Łukasz Fijałkowski</author><author>Saba Riaz</author><author>Amer Jamil</author>
        <description><![CDATA[Studies have identified specific salivary biomarkers associated with different types of cancer, including oral, lung, and pancreatic cancers. These biomarkers can be proteins, DNA fragments, or other molecules that indicate the presence or progression of the disease. Saliva-based cancer detection offers the potential for earlier diagnosis, leading to better treatment outcomes. Additionally, salivary biomarkers can help tailor treatment plans to individual patients, improving their chances of successful recovery.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/abp.2025.14935</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/abp.2025.14935</link>
        <title><![CDATA[Modulation of inflammatory and adrenergic pathways in hypertension: effects of β-blockers on cytokine release in Jurkat T cells]]></title>
        <pubdate>2025-10-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nana Kajaia</author><author>Maia Enukidze</author><author>Marine Machavariani</author><author>Tinatin Maminaishvili</author><author>Sophio Kalmakhelidze</author><author>George Ormotsadze</author><author>Tamar Sanikidze</author>
        <description><![CDATA[Research aimed to examine the effects of β-blockers on cytokine release in Jurkat cells under basal conditions and during oxidative stress. Oxidative stress was induced in Jurkat cells through the application of hydrogen peroxide (H2O2). Subsequently, β-blockers were administered to the incubation medium for 24 h, encompassing both intact and oxidatively stressed cell conditions. For β-blocker toxicity screening, the viability of Jurkat cells was determined using the MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) test. The IL-6, IL-17, and TNF-α content were measured in the supernatant of Jurkat cells incubated under different conditions. The study results show that propranolol, metoprolol, carvedilol, but not nebivolol, revealed toxic effects on the intact Jurkat cells (pc-p = 0.0001; pc-m > 0.0001; pc-c = 0.0003; pc-n = 0.0525). Under oxidative stress conditions, the viability of Jurkat cells decreased significantly (pc-H2O2 = 0.0001). Propranolol and metoprolol did not affect ((pc-p = 0.0001; pc-m > 0.0001), while nebivolol and carvedilol improved the viability of Jurkat cells incubated under oxidative stress conditions (pc-n = 0.002; pc-c = 0.0002). Oxidative stress significantly increased the cytokines (IL-6, TNF-α, IL-17) expression levels (pc-H2O2 < 0.0001; pc-H2O2 < 0.0001; pc-H2O2 < 0.0001) in Jurkat cells. Propranolol, carvedilol, nebivolol, and metoprolol did not significantly affect the expression levels of IL-6, TNF-α, and IL-17 in intact Jurkat cells, but decreased IL-6, TNF-α, and did not change IL-17 expression levels in Jurkat cells incubated under oxidative stress conditions. This study demonstrates that β-blockers can influence redox-sensitive cytokine pathways in Jurkat T lymphocytes when they are under oxidative stress. All the agents tested inhibited the production of IL-6 and TNF-α, but nebivolol and carvedilol showed the strongest protective and anti-inflammatory effects. These effects likely result from their combined properties, including antioxidant effects, nitric oxide modulation, and the regulation of NF-κB/MAPK pathways. In contrast, propranolol and metoprolol exhibited more limited activity. These findings suggest that third-generation β-blockers may offer both cardiovascular and immunomodulatory benefits, although further validation in primary immune cells and in vivo models is still required.]]></description>
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