
Hyperglycemia and increased activity of the renal angiotensin II (ANG II) system are two primary pathogenic stimuli for the onset and progression of podocyte injury in diabetic nephropathy. The study demonstrated that high glucose (HG) enhanced podocyte SOCE. It is also known that ANG II activates SOCE by releasing endoplasmic reticulum Ca2+. The present study aimed to determine whether enhanced SOCE-mediated HG- and ANG II-induced podocyte apoptosis and mitochondrial damage. In the kidneys of mice with diabetic nephropathy, the number of podocytes was significantly reduced. This study tested the hypothesis that overwhelming store-operated Ca2+ entry is a novel mechanism contributing to high glucose- and angiotensin II-induced podocyte apoptosis and mitochondrial injury.
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