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Fibrosis

Pericyte MyD88 and IRAK4 signalling in fibrosis

Nature Reviews Nephrology volume 13, page 63 (2017)Cite this article

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Pharmacological inhibition of IRAK4 signalling suppresses inflammatory and fibrotic markers

New data suggest that signalling of MyD88 and its downstream effector IRAK4 in pericytes is an important driver of inflammation and fibrogenesis in the injured kidney. Jeremy Duffield and colleagues also show that pharmacological inhibition of IRAK4 signalling suppresses inflammatory and fibrotic markers in kidney tissue of mice following ischaemia–reperfusion injury (IRI), suggesting that this pathway might represent a therapeutic avenue for the treatment of renal fibrosis.

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References

  1. Leaf, I. A. et al. Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury. J. Clin. Invest. http://dx.doi.org/10.1172/JCI87532 (2016)

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  1. Susan J. Allison
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Allison, S. Pericyte MyD88 and IRAK4 signalling in fibrosis. Nat Rev Nephrol 13, 63 (2017). https://doi.org/10.1038/nrneph.2016.174

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