Fibroblast-Specific Depletion of Human Antigen R Alleviates Myocardial Fibrosis Induced by Cardiac Stress

Mallikarjun Patil, Sarojini Singh, Praveen Kumar Dubey, Sultan Tousif, Prachi Umbarkar, Qinkun Zhang, Hind Lal, Mary Kathryn Sewell-Loftin, Channakeshava Sokke Umeshappa, Yohannes T. Ghebre, Steven Pogwizd, Jianyi Zhang, Prasanna Krishnamurthy

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Cardiac fibrosis can be mitigated by limiting fibroblast-to-myofibroblast differentiation and proliferation. Human antigen R (HuR) modulates messenger RNA stability and expression of multiple genes. However, the direct role of cardiac myofibroblast HuR is unknown. Myofibroblast-specific deletion of HuR limited cardiac fibrosis and preserved cardiac functions in pressure overload injury. Knockdown of HuR in transforming growth factor-β1–treated cardiac fibroblasts suppressed myofibroblast differentiation and proliferation. HuR deletion abrogated the expression and messenger RNA stability of cyclins D1 and A2, suggesting a potential mechanism by which HuR promotes myofibroblast proliferation. Overall, these data suggest that inhibition of HuR could be a potential therapeutic approach to limit cardiac fibrosis.

Original languageEnglish (US)
Pages (from-to)754-770
Number of pages17
JournalJACC: Basic to Translational Science
Issue number6
StatePublished - Jun 2024


  • cardiac fibrosis
  • heart failure
  • human antigen R
  • left ventricular remodeling
  • myofibroblasts

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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