Fig. 9. A potential mechanism by which Mas mediates PA/high-fat-induced impaired autophagy flux and ER stress in proximal tubular cells.

Activation of Mas resulted in increased intracellular calcium levels, via incompletely degradated VDAC1 due to failure in binding to P62 and ubiquitin, causing mitochondrial damage and accumulation of autophagosomes, which induces ER stress and apoptosis.