Runx1 in Postn-Expressing Fibroblasts But Not Cardiomyocytes Exacerbates Adverse Cardiac Remodeling Post-Myocardial Infarction

Runx1 is strongly induced in the heart after acute injury and in chronic disease settings. Its expression negatively correlates with outcomes, and past work demonstrates a protective effect when Runx1 is inhibited through a variety of experimental means. We sought to establish which Runx1-expressing cell type(s) are responsible for the adverse remodeling phenotypes observed upon its induction. Using distinct Cre drivers, we ablated Runx1 from cardiomyocytes and fibroblasts. Following experimental myocardial infarction, we established that loss of Runx1 in fibroblasts, but not cardiomyocytes, is able to protect from adverse remodeling.

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Publication Details

Journal
JACC Basic to Translational Science
Published
2026-01-13
DOI
https://doi.org/10.1016/j.jacbts.2025.101455
Primary Topic
Cardiac Fibrosis and Remodeling
Type
article
Field-Weighted Citation Impact
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article

Runx1 in Postn-Expressing Fibroblasts But Not Cardiomyocytes Exacerbates Adverse Cardiac Remodeling Post-Myocardial Infarction

Alexandra L. Purdy, Michaela Patterson, Michael A. Flinn, Anooj Arkatkar et al.
JACC Basic to Translational Science
Cardiac Fibrosis and Remodeling
article

Runx1 in Postn-Expressing Fibroblasts But Not Cardiomyocytes Exacerbates Adverse Cardiac Remodeling Post-Myocardial Infarction

Alexandra L. Purdy, Michaela Patterson, Michael A. Flinn, Anooj Arkatkar, Brian L. Lin, Kaelin A. Akins, Samantha Swift, Miao Cui, Sydney L. Buday, Annabelle Brusacoram, Priyanka Choudhury, Natalie Sandor, Caitlin C. O’Meara
article en

Abstract

Runx1 is strongly induced in the heart after acute injury and in chronic disease settings. Its expression negatively correlates with outcomes, and past work demonstrates a protective effect when Runx1 is inhibited through a variety of experimental means. We sought to establish which Runx1-expressing cell type(s) are responsible for the adverse remodeling phenotypes observed upon its induction. Using distinct Cre drivers, we ablated Runx1 from cardiomyocytes and fibroblasts. Following experimental myocardial infarction, we established that loss of Runx1 in fibroblasts, but not cardiomyocytes, is able to protect from adverse remodeling.

JACC Basic to Translational ScienceVol. 11(2)
Boston Children's Hospital (US), Medical College of Wisconsin (US)
Good health and well-being
Openalex Percentile: Top 89%
Cardiac Fibrosis and Remodeling
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