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Diabetic nephropathy

MiR-23b protects against fibrosis in diabetic nephropathy

Nature Reviews Nephrology volume 12, page 197 (2016)Cite this article

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Zhao and colleagues found that miR-23b was downregulated in the serum of patients with diabetes mellitus compared with healthy individuals. In diabetic murine kidneys and in cultured human embryonic kidney cells exposed to high glucose levels, miR-23b was also downregulated, whereas mRNA levels of G3bp2 were increased compared with controls. Moreover, in vitro inhibition of p38MAPK upregulated miR-23b, whereas inhibition of G3BP2 or overexpression of miR-23b downregulated p38MAPK in high-glucose conditions. Further analyses confirmed that miR-23b is a negative regulator of G3BP2, and identified a binding site for p53 — a downstream target of p38MAPK signalling — in the miR-23b promoter.

overexpression of miR-23b ... reversed renal fibrosis and reduced albuminuria in diabetic mice

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References

  1. Zhao, B. et al. MicroRNA-23b targets RAS GTPase-activating protein SH3 domain-binding protein 2 to alleviate fibrosis and albuminuria in diabetic nephropathy. J. Am. Soc. Nephrol. http://dx.doi.org/10.1681/ASN.2015030300

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  1. Ellen F. Carney
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Carney, E. MiR-23b protects against fibrosis in diabetic nephropathy. Nat Rev Nephrol 12, 197 (2016). https://doi.org/10.1038/nrneph.2016.22

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