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Targeting RUNX1 protects against diastolic dysfunction in a two-hit mouse model of heart failure with preserved
Ali Ali Mohamed Elbassioni1,2, Anmar A Raheem1, Jian Song1
1School of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK.
Cardiovascular Research
|May 26, 2026
Summary
Targeting the RUNX1 transcription factor can limit adverse cardiac remodeling in heart failure with preserved ejection fraction (HFpEF). This research presents RUNX1 as a novel therapeutic target for treating HFpEF.
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Heart failure with preserved ejection fraction (HFpEF) is increasingly prevalent with limited therapeutic options.
- HFpEF is a systemic condition characterized by diastolic dysfunction, pulmonary edema, exercise intolerance, and left ventricular hypertrophy.
- The role of the transcription factor RUNX1 in HFpEF pathogenesis was previously unknown.
Purpose of the Study:
- To investigate the role of RUNX1 in HFpEF.
- To determine if targeting RUNX1 could be a therapeutic strategy for HFpEF.
Main Methods:
- Utilized a clinically relevant mouse model of HFpEF.
- Generated cardiomyocyte-specific tamoxifen-inducible Runx1-deficient mice.
- Administered gene transfer or the small molecule inhibitor Ro5-3335 to target RUNX1.
Main Results:
- Inhibition of Runx1 limited adverse cardiac remodeling in HFpEF mice.
- Runx1 deficiency preserved diastolic function and attenuated pulmonary edema, exercise intolerance, and hypertrophy.
- Targeting RUNX1 improved diastolic function and reduced pulmonary edema in both male and female HFpEF mice.
Conclusions:
- RUNX1 plays a significant role in the pathophysiology of HFpEF.
- Targeting RUNX1 offers a novel therapeutic approach for HFpEF treatment.
