Mitochondria, endothelial cell function, and vascular diseases

Abstract

Mitochondria are perhaps the most sophisticated and dynamic responsive sensing systems in eukaryotic cells. The role of mitochondria goes beyond their capacity to create molecular fuel and includes the generation of reactive oxygen species, the regulation of calcium, and the activation of cell death. In endothelial cells, mitochondria have a profound impact on cellular function under both healthy and diseased conditions. In this review, we summarize the basic functions of mitochondria in endothelial cells and discuss the roles of mitochondria in endothelial dysfunction and vascular diseases, including atherosclerosis, diabetic vascular dysfunction, pulmonary artery hypertension, and hypertension. Finally, the potential therapeutic strategies to improve mitochondrial function in endothelial cells and vascular diseases are also discussed, with a focus on mitochondrial-targeted antioxidants and calorie restriction.

Mitochondrial Sirtuins and Their Relationships with Metabolic Disease and Cancer

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Sirt3–MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts

“…Mitochondria are one of the main sources of ROS. The inhibition of mitochondrial ROS is considered to be better than global ROS inhibition for therapy of diverse disorders [10]. Mitochondria oxidative stress and dysfunction essentially contribute to osteoporosis through regulating processes including mitophagy, apoptosis, and mitochondrial DNA (mtDNA) damage [11][12][13].…”

Loading MiR-210 in Endothelial Progenitor Cells Derived Exosomes Boosts Their Beneficial Effects on Hypoxia/Reoxygeneation-Injured Human Endothelial Cells via Protecting Mitochondrial Function

“…Mitochondria are essential organelles and play a significant role in a wide range of cells, including ECs and cardiomyocytes [22][23][24]. EC injury induced by ischemia-reperfusion and EC dysfunction in diabetes mellitus are associated with mitochondrial ROS overproduction [25] and mitochondrial fragmentation [24].…”