Why the study?
Fibrosis is a hallmark of cardiorenal disease with no specific anti-fibrotic treatments currently available.
Does targeting IL-11 prevent or reduce cardiac and renal fibrosis in preclinical models?
Does targeting IL-11 prevent or reduce cardiac and renal fibrosis in preclinical models?
IL-11 has emerged as a critical, non-redundant driver of cardiorenal fibrosis, offering a promising new therapeutic target.
IL-11 inhibition merits human trials in cardiorenal fibrosis; leaves open whether preclinical protection translates to clinical outcomes.
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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Corden et al. (2020) studied this question.
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