Key result
Dietary nitrate improves cardiac function and reduces fibrosis and inflammation in HFrEF mouse models.
Why the study?
Dietary nitrate restores nitric oxide levels and may offer cardioprotection, but its long-term impact on HFrEF remains unclear.
Does dietary nitrate supplementation improve cardiac function and reduce adverse remodeling in mouse models of HFrEF?
Does dietary nitrate supplementation improve cardiac function and reduce adverse remodeling in mouse models of HFrEF?
Dietary nitrate supplementation improves cardiac and vascular function while reducing fibrosis and inflammation in preclinical models of HFrEF, highlighting its potential as a cardioprotective therapy.
No change to HFrEF care indicated; leaves open translation of nitrate benefits to patients.
Background Heart failure with reduced ejection fraction (HFrEF) is characterized by impaired cardiac function, reduced nitric oxide (NO) availability, and dysregulated immune responses, which contribute to adverse cardiac remodeling and disease progression. Dietary nitrate has been shown to restore NO levels and may offer cardioprotective effects, though its long-term impact on HFrEF remains unclear. Purpose This study aimed to investigate the potential of dietary nitrate supplementation to prevent adverse cardiac remodeling, improve cardiac function, and reduce fibrosis and inflammation in HFrEF. Methods Two mouse models of HFrEF, induced by myocardial infarction (MI) or transverse aortic constriction (TAC), were treated with dietary nitrate or a control diet, starting three days post-surgery for 4-6 weeks. Cardiac function and hemodynamics were assessed using echocardiography and pressure-volume (PV) loop analysis. Cardiac fibrosis was evaluated via histology, and ex vivo aortic vasorelaxation was measured through myograph experiments. Molecular markers related to hypertrophy, fibrosis, and inflammation were analyzed via quantitative PCR (Q-PCR). Results Nitrate supplementation improved systolic and diastolic cardiac function, enhanced aortic vasorelaxation, and reduced both replacement and reactive fibrosis. Additionally, it decreased transcriptional markers linked to hypertrophy, fibrosis, and inflammation, while promoting anti-inflammatory macrophage polarization. Conclusion Dietary nitrate supplementation shows promise as a cardioprotective therapy by improving cardiac and vascular function, reducing fibrosis, and modulating inflammation, thus slowing the progression of HFrEF.
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Shimari et al. (2025) studied Heart failure with reduced ejection fraction (HFrEF). Dietary nitrate vs. Control diet was evaluated on Cardiac function, hemodynamics, cardiac fibrosis, and inflammation. Dietary nitrate supplementation improved systolic and diastolic cardiac function, enhanced aortic vasorelaxation, and reduced fibrosis and inflammation in mouse models of HFrEF.
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