MicroRNAs for podocyte injury in diabetic nephropathy
Diabetic nephropathy is one of critical complications of diabetes mellitus. It can progress to end-stage renal disease, which requires renal replacement therapy. Podocyte injury contributes to the development and progression of diabetic nephropathy (1,2). However, the pathogenesis and regulatory molecules for podocyte injury have not been fully clarified.
MicroRNAs are small, non-coding, single-stranded RNAs that have been identified as essential regulators for the expression levels of many target mRNAs through degradation or suppression of translation by RNA interference (3). Although some microRNAs that regulate podocyte injury in diabetic nephropathy have been reported (4), further studies are warranted because many unreported microRNAs and their target mRNAs may play pivotal roles for podocyte injury in diabetic nephropathy.
Li et al. (5) showed that the microRNA-30 family members contribute to podocyte injury in diabetic nephropathy through the regulation of apoptosis and endoplasmic reticulum stress by modulating the expression level of connexin-43, an essential molecule for coordinated kidney function in cultured podocyte cells in vitro and diabetic nephropathy model rats in vivo.
These findings encourage further progression in studies on microRNAs for podocyte injury in diabetic nephropathy. The findings may also lead to the development of new pharmacological drugs and the identification of novel biomarkers for podocyte injury in diabetic nephropathy.
Acknowledgments
Funding: None.
Footnote
Provenance and Peer Review: This article was commissioned by the editorial office, Annals of Translational Medicine. The article did not undergo external peer review.
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- Li M, Ni W, Zhang M, et al. MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy. Ann Transl Med 2020;8:1674. [Crossref] [PubMed]