Endocrine Regulation of Mitochondrial Function and Redox Signaling in Cardiovascular Disease

Mitochondrial dysfunction and redox imbalance are central drivers of cardiovascular disease, contributing to impaired bioenergetics, oxidative stress, inflammation, and adverse cardiac and vascular remodeling. Increasing evidence indicates that these processes are tightly regulated by endocrine signaling pathways, including insulin and IGF signaling, thyroid hormone, the renin–angiotensin–aldosterone system (RAAS), peroxisome proliferator-activated receptors (PPARs), adipokines, and sex steroids. However, the integration of endocrine regulation with mitochondrial and redox biology remains fragmented across disciplines, limiting mechanistic insight and translational progress.This Research Topic aims to define how endocrine signals reprogram mitochondrial function and redox homeostasis to shape cardiovascular phenotypes across health and disease. We welcome basic, translational, and clinical studies that investigate mitochondrial dynamics, including fusion–fission balance, mitophagy pathways such as PINK1–Parkin, calcium handling, substrate utilization, and oxidative phosphorylation efficiency, as well as reactive oxygen and nitrogen species signaling and inflammasome activation. Particular emphasis will be placed on linking endocrine pathways to cardiovascular outcomes, including heart failure, ischemia–reperfusion injury, hypertrophy, endothelial dysfunction, arrhythmia susceptibility, and cardiometabolic disease.We encourage submissions leveraging multi-omics approaches, advanced imaging, high-resolution respirometry, human genetics, and longitudinal cohort studies to elucidate endocrine–mitochondrial crosstalk. Interventional and mechanistic studies examining endocrine and cardiometabolic therapies, including SGLT2 inhibitors, GLP-1 receptor agonists, mineralocorticoid receptor antagonists, thyroid and PPAR modulators, as well as exercise and nutritional interventions, are particularly welcome, especially where mitochondrial or redox endpoints are assessed.We welcome contributions addressing, but not limited to, the following themes:• Endocrine regulation of mitochondrial dynamics, including fusion, fission, and mitophagy• Hormonal control of mitochondrial bioenergetics and substrate utilization• Redox signaling, oxidative stress, and inflammasome activation in cardiovascular disease• Interactions between endocrine pathways and mitochondrial calcium handling• Adipokines, sex steroids, and thyroid hormones in mitochondrial remodeling• RAAS and mineralocorticoid signaling in mitochondrial and vascular dysfunction• Mitochondrial dysfunction in heart failure, ischemia–reperfusion injury, and cardiometabolic disease• Multi-omics and systems biology approaches to endocrine–mitochondrial crosstalk• Biomarkers of mitochondrial dysfunction and redox imbalance in cardiovascular disease• Therapeutic targeting of mitochondrial and redox pathways in cardiovascular endocrinologyBy integrating endocrine signaling with organelle-level mechanisms, this Research Topic aims to advance a more unified understanding of mitochondrial and redox regulation in cardiovascular disease and to identify actionable pathways for precision prevention and therapy. Topic editors: Antonietta Franco, Gokhan Burcin Kubat Source: https://www.frontiersin.org/research-topics/81489/endocrine-regulation-of-mitochondrial-function-and-redox-signaling-in-cardiovascular-disease