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Renal fibrosis

Activation of JAK3/STAT6 contributes to the development of renal fibrosis

Nature Reviews Nephrology volume 11, page 445 (2015)Cite this article

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Bone marrow-derived fibroblast precursors (fibrocytes) contribute to the pathogenesis of renal fibrosis, but the mechanisms that underlie their activation and recruitment to the kidney are not fully understood. Now, data from Jingyin Yan and colleagues implicate JAK3/STAT6 signalling in fibrocyte activation.

The researchers detected activated STAT6 in bone marrow-derived monocytes after culturing them in the presence of the profibrotic cytokines IL–4 and IL–13. These cytokines also enhanced the expression of extracellular matrix (ECM) proteins and α-SMA, which were attenuated upon application of the JAK3-specific inhibitor, CP690,550, as well as in bone marrow-derived monocytes isolated from STAT6−/− mice.

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References

  1. Yan, J. et al. JAK3/STAT6 stimulates bone marrow-derived fibroblast activation in renal fibrosis. J. Am. Soc. Nephrol. 10.1681/ASN.2014070717

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  1. Jessica K. Edwards
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Edwards, J. Activation of JAK3/STAT6 contributes to the development of renal fibrosis. Nat Rev Nephrol 11, 445 (2015). https://doi.org/10.1038/nrneph.2015.97

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