Autophagy behavior in Endothelial Cell Dysfunction

Autophagy regulates endothelial cell homeostasis. Autophagy is a catabolic process involving degradation of intracellular components. Dysregulation of autophagy induces endothelial cell dysfunction. Endothelial cell dysfunction is a multifactorial pathophysiological change that occurs at the cellular and subcellular levels. Lipophagy and mitophagy are hallmarks of the pathogenesis of endothelial cell dysfunction. The regulation of the autophagy mechanism involved amino acids, growth factors, hormones, myo-inositol-1,4,5-triphosphate, calpain, calcium, bcl-2, reactive oxygen species, BNIP3, DRAM, p19ARF, FADD and TRAIL. Down-regulation of autophagy reduces endothelial cell resistance to stressful conditions such as shear stress, deprivation of oxidative stress, nutrients deprivation, and hypoxemia. Autophagy optimizes endothelial cell function, increases longevity, slows senescence, and prevents endothelial cell transdifferentiation. Pathophysiologically, autophagy is inhibited in endothelial cells due to mTORC1 repression release. Also, AMPK expression repression downregulates autophagy and subsequently endothelial dysfunction. The paper provides state of art on the current advances in the autophagy role in endothelial cell dysfunction.