Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
October 9, 2025Circulation Research

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

View Full Paper
Ask AI
Bookmark
Share

Authors

JPJ. PindaroMFM. W. FlinnSÁSantiago Álvarez

Discussion

Loading...

Member takes

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
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Myofibroblast Ccn3 is regulated by Yap and Wwtr1 and contributes to adverse cardiac outcomes2023 · 10 citations
  2. 2Myofibroblast Ccn3 is regulated by Yap and Wwtr1 and contributes to adverse cardiac outcomes2022 · 1 citations
  3. 3Single-Cell RNA Sequencing Analysis Reveals a Crucial Role for CTHRC1 (Collagen Triple Helix Repeat Containing 1) Cardiac Fibroblasts After Myocardial Infarction2020 · 275 citations
  4. 4Single-cell RNA sequencing reveals the potential role of Postn(+) fibroblasts in promoting the progression of myocardial fibrosis after myocardial infarction2025 · 12 citations
  5. 5Cardiac Fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction2018 · 18 citations