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October 9, 2025Circulation Research

Abstract Thu138: Myofibroblast CCN3 Contributes to Adverse Outcomes Following Myocardial Infarction

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Authors

JPJ. PindaroMFM. W. FlinnSÁSantiago Álvarez

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Overview

Conditional knockout of CCN3 in myofibroblasts improves cardiac function after myocardial infarction, suggesting potential therapeutic targets.

Key Points

  • Knockout of myofibroblast CCN3 leads to reduced cardiac fibrosis and scarring after myocardial infarction.
  • Administration of recombinant human CCN3 worsens cardiac function and fibrosis if given within three days post-injury.
  • Specific deletion of CCN3 in myofibroblasts improves overall cardiac function compared to control mice.
  • Understanding CCN3's pathways post-myocardial infarction may reveal novel therapeutic targets.

Cite This Study

Pindaro et al. (2025) studied this question.

synapsesocial.com/papers/68e77f09d1c187e1c108fbcchttps://doi.org/10.1161/res.137.suppl_1.thu138
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