Endothelial Autophagy Dysregulation in Diabetes

卷:12

Review

关键词: OXIDATIVE STRESS;    SHEAR-STRESS;    HIGH-GLUCOSE;    TRANSENDOTHELIAL MIGRATION;    LC3 LIPIDATION;    END-PRODUCTS;    PROTEIN;    CELLS;    COMPLEX;    MITOCHONDRIA;   

DOI  :  10.3390/cells12060947

来源: SCIE

【 摘 要 】

Diabetes mellitus is a major public health issue that affected 537 million people worldwide in 2021, a number that is only expected to increase in the upcoming decade. Diabetes is a systemic metabolic disease with devastating macro- and microvascular complications. Endothelial dysfunction is a key determinant in the pathogenesis of diabetes. Dysfunctional endothelium leads to vasoconstriction by decreased nitric oxide bioavailability and increased expression of vasoconstrictor factors, vascular inflammation through the production of pro-inflammatory cytokines, a loss of microvascular density leading to low organ perfusion, procoagulopathy, and/or arterial stiffening. Autophagy, a lysosomal recycling process, appears to play an important role in endothelial cells, ensuring endothelial homeostasis and functions. Previous reports have provided evidence of autophagic flux impairment in patients with type I or type II diabetes. In this review, we report evidence of endothelial autophagy dysfunction during diabetes. We discuss the mechanisms driving endothelial autophagic flux impairment and summarize therapeutic strategies targeting autophagy in diabetes.