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September 11, 2025Science

Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy

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Authors

RBRoss C. BrethertonIRIsabella M. ReichardtKZKristin A. Zabrecky

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Overview

Observational analysis shows fibroblast activity modifies DCM phenotypes in mice, indicating p38 deletion may improve contractility.

Key Points

  • Cardiac fibroblast expansion contributes to dilated cardiomyopathy, altering disease severity and myocardium stiffness.
  • The study observed that p38 deletion in DCM mice prevented fibroblast responses and improved cardiomyocyte contractility.
  • Fibroblast states were mechanosensitized, indicating their role in the early stages of cardiac remodeling and fibrosis.
  • Targeting fibroblast responses offers a new potential approach for therapy in managing dilated cardiomyopathy.

Cite This Study

Bretherton et al. (2025) studied this question.

synapsesocial.com/papers/68d41405713b0b5dfea624afhttps://doi.org/10.1126/science.adv9157
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