ArticleCardiovascular research2026
Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved ejection fraction.
Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- SOX2-OT serves as a diagnostic and prognostic biomarker for hypertensive left ventricular hypertrophy by targeting miR-30d-5p.Molecular and cellular biochemistry · 2026Article
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29 authors.
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Abstract
aimsHeart failure with preserved ejection fraction (HFpEF) continues to increase in prevalence and has limited treatment options. HFpEF is a systemic condition with a broad phenotype including diastolic dysfunction, pulmonary oedema, exercise intolerance, and left ventricular hypertrophy, collectively resulting in enhanced morbidity and mortality. The transcription factor RUNX1 has recently been identified as a mediator of pathological changes in multiple cardiac diseases; however, its role in HFpEF remained unknown. METHODS AND
resultsHere, we show that inhibition of Runx1 limits adverse cardiac remodelling in a mouse model of HFpEF. Cardiomyocyte-specific tamoxifen-inducible Runx1-deficient mice with HFpEF are protected, with preservation of diastolic function, and attenuation of pulmonary oedema, exercise intolerance, and hypertrophy. Furthermore, targeting Runx1 in HFpEF by using gene transfer or small-molecule inhibitor Ro5-3335 improves diastolic function and reduces pulmonary oedema, both in female and male mice.
conclusionOverall, this work enhances our understanding of RUNX1 in cardiac disease and presents a novel translational target for the treatment of HFpEF.
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