Experimental and Molecular Medicine (Aug 2019)

Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1

  • Dong-Wei Liu,
  • Jia-Hui Zhang,
  • Feng-Xun Liu,
  • Xu-Tong Wang,
  • Shao-Kang Pan,
  • Deng-Ke Jiang,
  • Zi-Hao Zhao,
  • Zhang-Suo Liu

DOI
https://doi.org/10.1038/s12276-019-0259-6
Journal volume & issue
Vol. 51, no. 8
pp. 1 – 15

Abstract

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Diabetic kidney disease: Improving treatment by targeting an RNA molecule Targeting an RNA molecule responsible for disrupting metabolic protein levels in diabetic kidney disease may improve treatment. Diabetic nephropathy (DN) can affect people with type I or type II diabetes, and results in functional deterioration and the need for regular dialysis. DN incidence is rising worldwide, but existing treatments are only partially effective. Zhang-Suo Liu at Zhengzhou University, China, and co-workers examined the role of a long noncoding RNA molecule known as PVT1, which has been recently associated with kidney disease. The team collected serum samples from 32 patients with DN, and also generated a DN mouse model. They found that PVT1 expression was significantly higher in DN, and that this inhibited the expression of a key metabolic protein, FOXA1. Silencing PVT1 restored FOXA1 levels, limiting damage and cell death in kidney cells.