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Notch 通路通过 Bcl-2 和 p53 通路参与高糖诱导的足细胞凋亡。

Notch pathway is involved in high glucose-induced apoptosis in podocytes via Bcl-2 and p53 pathways.

机构信息

Department of Pathology, Hebei Medical University, Shijiazhuang, Hebei 050017, China.

出版信息

J Cell Biochem. 2013 May;114(5):1029-38. doi: 10.1002/jcb.24442.

DOI:10.1002/jcb.24442
PMID:23129176
Abstract

Recent studies have shown that Notch pathway plays a key role in the pathogenesis of diabetic nephropathy (DN), however, the exact mechanisms remain elusive. Here we demonstrated that high glucose (HG) upregulated Notch pathway in podocytes accompanied with the alteration of Bcl-2 and p53 pathways, subsequently leading to podocytes apoptosis. Inhibition of Notch pathway by chemical inhibitor or specific short hairpin RNA (shRNA) vector in podocytes prevented Bcl-2- and p53-dependent cell apoptosis. These findings suggest that Notch pathway mediates HG-induced podocytes apoptosis via Bcl-2 and p53 pathways.

摘要

最近的研究表明,Notch 通路在糖尿病肾病 (DN) 的发病机制中起着关键作用,然而,确切的机制仍不清楚。在这里,我们证明高葡萄糖 (HG) 可使足细胞中的 Notch 通路上调,同时伴随着 Bcl-2 和 p53 通路的改变,进而导致足细胞凋亡。用化学抑制剂或特异性短发夹 RNA (shRNA) 载体抑制 Notch 通路可防止 Bcl-2 和 p53 依赖性细胞凋亡。这些发现表明,Notch 通路通过 Bcl-2 和 p53 通路介导 HG 诱导的足细胞凋亡。

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