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Cardiac fibrosis

Dual mechanotherapy for the treatment of cardiac fibrosis

Nature Reviews Cardiology volume 22, page 465 (2025)Cite this article

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Inhibition of mechanotransduction selectively in cardiac fibroblasts, especially when combined with inhibition of transforming growth factor-β (TGFβ) signalling, triggers a reversal of fibroblast activation and suppresses fibrosis in diseased hearts, according to findings published in Nature. “We demonstrate that targeting the stroma-enriched mechanosensor SRC can recapitulate the effects of extracellular matrix softening selectively in stromal cells, essentially allowing us to ‘trick’ the cells into perceiving a stiff, fibrotic environment as soft,” highlight study investigators Sangkyun Cho and Joseph Wu. “Our study builds on the growing body of work that suggests that fibroblast activation states can be readily modulated not just by soluble (for example, pro-inflammatory) signals, but also by mechanical cues from the fibrotic niche,” they add.

First, the investigators performed a meta-analysis of publicly available single-cell RNA-sequencing data from humans and mice and identified a druggable mechanosensor that is particularly enriched and activated in cardiac fibroblasts and that could be targeted to mimic the effects of extracellular matrix softening: the focal adhesion-associated tyrosine-protein kinase SRC, which is a signal transducer upstream of YAP–TAZ.

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  • Frangogiannis, N. G. Transforming growth factor-β in myocardial disease. Nat. Rev. Cardiol. 19, 435–455 (2022)

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  1. Nature Reviews Cardiology http://www.nature.com/nrcardio/

    Irene Fernández-Ruiz

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  1. Irene Fernández-Ruiz
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Correspondence to Irene Fernández-Ruiz.

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Fernández-Ruiz, I. Dual mechanotherapy for the treatment of cardiac fibrosis. Nat Rev Cardiol 22, 465 (2025). https://doi.org/10.1038/s41569-025-01172-9

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