Key result
H2S donor supplementation improves diastolic function and reduces cardiac fibrosis in preclinical HFpEF models.
Why the study?
Does pharmacological supplementation with an H2S donor improve diastolic function and reduce cardiac fibrosis in models of HFpEF?
Does pharmacological supplementation with an H2S donor improve diastolic function and reduce cardiac fibrosis in models of HFpEF?
Enhancing hydrogen sulfide bioavailability improves diastolic function and reduces cardiac fibrosis in preclinical models of HFpEF, representing a potential novel therapeutic strategy.
Heart failure with preserved ejection fraction (HFpEF) presents significant treatment challenges. We assessed hydrogen sulfide (H2S) bioavailability in HFpEF patients and 2 animal models: the "2-hit" L-NAME + high-fat diet mouse model and ZSF1 obese rats. H2S levels were significantly reduced in patients and both models, linked to decreased cystathionine-γ-lyase expression and increased sulfide quinone oxidoreductase. Cystathionine-γ-lyase knockout worsened HFpEF, whereas pharmacological supplementation with an H2S donor improved diastolic function and reduced cardiac fibrosis. H2S supplement synergized with GLP-1/glucagon agonist and ameliorated HFpEF. These findings suggest that enhancing H2S bioavailability may provide a novel therapeutic strategy for HFpEF.
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Doiron et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF). Hydrogen sulfide (H2S) donor supplementation was evaluated on Diastolic function and cardiac fibrosis. Pharmacological supplementation with an H2S donor improved diastolic function and reduced cardiac fibrosis in animal models of HFpEF.
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