Mitochondria are dynamic organelles central to cellular homeostasis, providing energy through ATP production while regulating calcium signalling, redox balance, apoptosis, and metabolic integration. Beyond bioenergetics, they serve as critical signalling hubs that coordinate cellular adaptation to stress.

Dysfunctional mitochondria generate excessive reactive oxygen species, disrupt metabolic and signalling networks, and contribute to tissue damage. Mounting evidence implicates mitochondrial impairment in the development of major chronic diseases, including diabetes, obesity, neurodegenerative disorders, cardiovascular diseases, and cancer.
In endothelial cells, mitochondrial dysfunction is particularly detrimental, driving inflammation, vascular stiffness, and metabolic imbalance, all of which exacerbate cardiometabolic risk. Consequently, elucidating the mechanisms that maintain or restore endothelial mitochondrial function has become a pivotal focus for developing innovative therapies to prevent or mitigate cardiovascular and metabolic disorders.

This Special Issue welcomes original research articles and comprehensive reviews that advance our understanding of endothelial mitochondrial biology in cardiovascular and metabolic diseases. We encourage submissions addressing molecular mechanisms of mitochondrial dysfunction, redox signalling, metabolic reprogramming, mitochondrial dynamics, mitophagy, and inter-organelle communication. Studies exploring novel therapeutic strategies targeting endothelial mitochondria—including pharmacological agents, genetic approaches, and lifestyle interventions—are particularly encouraged. Contributions employing translational, clinical, or multi-omics approaches that bridge basic mechanisms with disease outcomes are also highly valued.

Potential areas of interest may include, but are not limited to:
● Molecular mechanisms regulating endothelial mitochondrial bioenergetics, dynamics, and quality control
● Mitochondrial redox signalling and its role in vascular inflammation and metabolic dysfunction
● Crosstalk between endothelial mitochondria and other organelles in cardiometabolic disease
● Therapeutic strategies targeting mitochondrial pathways to prevent or reverse cardiovascular and metabolic disorders

Authors are welcome to submit articles presenting original studies or literature review work. Please consult the journal's information regarding Article Types, Author Guidelines, and Publishing Fees, or direct any questions to the Editorial Office: abp@frontierspartnerships.org.

Even though abstract submission is not mandatory, we encourage all interested researchers to submit a “manuscript summary” before submitting their article. Manuscript summaries do not have to coincide with the final abstract of the article.

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Acta Biochimica Polonica