Recently, the mitochondrion has been considered a central biological hub in developing cardiovascular diseases (CVDs), including (but not limited to) hypertension, atherosclerosis, myocardial infarction, cardiovascular aging, and heart failure. Mitochondria play various vital physiological and pathophysiological roles in most cell types of the cardiovascular system, regulating several interrelated cellular processes such as intracellular calcium handling, maintenance of metabolic homeostasis, inflammatory responses, redox signaling, and multiple cell death pathways. Physiologically, cardiovascular cells rely heavily on mitochondria for energy production through oxidative phosphorylation, and calcium flux is central to this process in cardiomyocytes and vascular smooth muscle cells. Also, endothelial cells are sensitive to pathogenic inflammatory responses triggered by damaged mitochondria. Thus, mitochondrial health is tightly related to cardiovascular homeostasis.
Mitochondria are sensors and integrators of environmental cues in pathophysiological conditions. Mitochondria typically form a strict and hierarchical quality control system controlled by a dynamic network. They also communicate with other organelles, such as the endoplasmic reticulum and nucleus. Despite the advances in mitochondrial biology and improved methods to monitor mitochondrial defects, we are still far from fully understanding the events relating to the organelle that drive cardiovascular disorders. In addition, no effective therapeutics, to date, are available clinically to mitigate mitochondria-associated dysfunctions. In this endeavor, studies are needed to elucidate different biological mechanisms linking mitochondria with CVDs, develop new tools for mitochondrial research, and explore new targets for mitochondria-based therapies.
In this research topic, we would like to collate articles that will extend our understanding of the molecular bases, methods, and therapeutic approaches involved in mitochondria-related CVDs. Therefore, we welcome Original Research, Methods, Review, and Mini-Review articles that cover, but are not limited to, the following topics:
• Genetic defects of mitochondria in cardiovascular diseases
• Biological bases of mitochondria involved in the pathogenesis of cardiovascular diseases, including myocardial infarction, cardiomyopathy, heart failure, hypertension, atherosclerosis, and other vascular diseases
• Novel function and mechanisms of mitochondria-related metabolism, calcium flux, mitochondrial dynamics, apoptosis, and ferroptosis
• mtDNA
• Mitochondrial targeting (MTA) therapy
• Mitochondrial alterations at the genetic, protein, and metabolite levels under extreme environment
Recently, the mitochondrion has been considered a central biological hub in developing cardiovascular diseases (CVDs), including (but not limited to) hypertension, atherosclerosis, myocardial infarction, cardiovascular aging, and heart failure. Mitochondria play various vital physiological and pathophysiological roles in most cell types of the cardiovascular system, regulating several interrelated cellular processes such as intracellular calcium handling, maintenance of metabolic homeostasis, inflammatory responses, redox signaling, and multiple cell death pathways. Physiologically, cardiovascular cells rely heavily on mitochondria for energy production through oxidative phosphorylation, and calcium flux is central to this process in cardiomyocytes and vascular smooth muscle cells. Also, endothelial cells are sensitive to pathogenic inflammatory responses triggered by damaged mitochondria. Thus, mitochondrial health is tightly related to cardiovascular homeostasis.
Mitochondria are sensors and integrators of environmental cues in pathophysiological conditions. Mitochondria typically form a strict and hierarchical quality control system controlled by a dynamic network. They also communicate with other organelles, such as the endoplasmic reticulum and nucleus. Despite the advances in mitochondrial biology and improved methods to monitor mitochondrial defects, we are still far from fully understanding the events relating to the organelle that drive cardiovascular disorders. In addition, no effective therapeutics, to date, are available clinically to mitigate mitochondria-associated dysfunctions. In this endeavor, studies are needed to elucidate different biological mechanisms linking mitochondria with CVDs, develop new tools for mitochondrial research, and explore new targets for mitochondria-based therapies.
In this research topic, we would like to collate articles that will extend our understanding of the molecular bases, methods, and therapeutic approaches involved in mitochondria-related CVDs. Therefore, we welcome Original Research, Methods, Review, and Mini-Review articles that cover, but are not limited to, the following topics:
• Genetic defects of mitochondria in cardiovascular diseases
• Biological bases of mitochondria involved in the pathogenesis of cardiovascular diseases, including myocardial infarction, cardiomyopathy, heart failure, hypertension, atherosclerosis, and other vascular diseases
• Novel function and mechanisms of mitochondria-related metabolism, calcium flux, mitochondrial dynamics, apoptosis, and ferroptosis
• mtDNA
• Mitochondrial targeting (MTA) therapy
• Mitochondrial alterations at the genetic, protein, and metabolite levels under extreme environment