What is it about?

Immune-mediated rapid destruction of the kidneys' filtering units or crescentic glomerulonephritis (CGN) is an exceptional condition where specific renal cells, the podocytes, undergo a dysregulation of their differentiated phenotype and transiently proliferate and migrate, resulting in the so-called “extracapillary glomerulopathy.” We demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with CGN. The CDK inhibitor p57Kip2 is a major target of miR-92a that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of miR-92a in mice de-repressed the expression of p57Kip2 and prevented glomerular injury in CGN.

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Why is it important?

We demonstrate for the first time that miRNA induction in epithelial cells can break glomerular tolerance to immune injury. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for CGN. Furthermore, we showed the feasibility and proof of concept of therapeutic inhibition of miR-92a in glomerular cells to prevent end-stage kidney disease.


These data support clinical studies to use miR-92a as a biomarker for severe CGN and trials to evaluate the clinical usefulness of anti-miR92a strategies.

MD, PhD Pierre-Louis Tharaux
Institut de la Santé et de la Recherche Médicale, Inserm

Read the Original

This page is a summary of: Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis, Nature Communications, November 2017, Springer Science + Business Media, DOI: 10.1038/s41467-017-01885-7.
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