| First Author | Li R | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 506 |
| Issue | 3 | Pages | 522-528 |
| PubMed ID | 30361092 | Mgi Jnum | J:270943 |
| Mgi Id | MGI:6276811 | Doi | 10.1016/j.bbrc.2018.10.081 |
| Citation | Li R, et al. (2018) Septin 7 mediates high glucose-induced podocyte apoptosis. Biochem Biophys Res Commun 506(3):522-528 |
| abstractText | Podocyte depletion is a central pathological mechanism of diabetic nephropathy (DN). Hyperglycemia induced podocyte apoptosis, resulting in podocyte depletion. However, the crucial mechanism of hyperglycemia-induced podocyte apoptosis remains poorly understood. In this study, we evaluated the expression of septin 7, a GTP-binding protein, in glomerular podocytes of patients and mice with DN, and investigated the pro-apoptotic effect of septin 7 on high glucose (HG) induced podocyte apoptosis in vitro. We found septin 7 expression was markedly increased not only in glomerular podocytes of patients and db/db mice with DN but also in cultured podocytes with HG stimulation. Knocking down septin 7 with siRNA could attenuate HG induced podocytes apoptosis and excessive intracellular Ca(2+) concentration. This study revealed septin7 may potentially play a proapoptotic role in podocyte under diabetic conditions and may provide a potential target for preventing podocyte apoptosis in DN. |
