Title:Autophagy Behavior in Endothelial Cell Dysfunction
Volume: 5
Author(s): Basheer Abdullah Marzoog*
Affiliation:
- Department of Normal and Pathological Physiology, National Research Mordovia State University, Bolshevitskaya Street, 68, Saransk, Rep.
Mordovia, 430005, Russia
Keywords:
Autophagy, Pathogenesis, Endothelial dysfunction, Atg8, Cell linage, Cell reprogramming.
Abstract: 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.
