Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 177, Issue 8, Pages 1695-1708Publisher
WILEY
DOI: 10.1111/bph.15013
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Funding
- MRC [MC_U120085815] Funding Source: UKRI
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Fibrosis is a pathophysiological hallmark of cardiorenal disease. In the heart, fibrosis leads to contractile dysfunction and arrhythmias; in the kidney, it is the final common pathway for many diseases and predicts end-stage renal failure. Despite this, there are currently no specific anti-fibrotic treatments available for cardiac or renal disease. Recently and unexpectedly, IL-11 was found to be of major importance for cardiorenal fibroblast activation and fibrosis. In mouse models, IL-11 overexpression caused fibrosis of the heart and kidney while genetic deletion of Il11ra1 protected against fibrosis and preserved organ function. Neutralizing antibodies against IL-11 or IL-11RA have been developed that have anti-fibrotic activity in human fibroblasts and protect against fibrosis in murine models of disease. While IL-11 biology has been little studied and, we suggest, largely misunderstood, its autocrine activity in myofibroblasts appears non-redundant for fibrosis, which offers new opportunities to better understand and potentially target cardiorenal fibrosis.
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