Key result
Oral nitazoxanide improves cardiac hypertrophy, diastolic dysfunction, and metabolic phenotypes in a HFpEF mouse model.
Why the study?
Because HFpEF pathogenesis is multifactorial and closely linked to diabetes, dyslipidemia, atherosclerosis, and inflammation, the authors investigated whether nitazoxanide protects against HFD plus L-NAME-induced HFpEF and metabolic syndrome.
Does nitazoxanide improve pathological phenotypes in a mouse model of HFpEF and metabolic syndrome?
Does nitazoxanide improve pathological phenotypes in a mouse model of HFpEF and metabolic syndrome?
Nitazoxanide protects against experimental HFpEF and metabolic syndrome in mice, suggesting potential therapeutic utility.
Supports nitazoxanide exploration in HFpEF models; leaves open translation to clinical practice.
The clinical antiprotozoal drug nitazoxanide has been demonstrated to improve the experimental diabetes mellitus, lipid metabolism disorders, atherosclerosis and inhibit inflammation. Since the pathogenesis of heart failure with preserved ejection (HFpEF) is multifactorial and closely associated with the aforementioned diseases, we aim to study the effect of nitazoxanide on high-fat diet (HFD) plus L-NAME (N ω -nitro-L-arginine methyl ester)-induced HFpEF and metabolic syndrome in mice. We found that oral nitazoxanide improved cardiac hypertrophy, cardiac fibrosis, cardiac diastolic dysfunction, increased blood pressure, impaired exercise tolerance, impaired glucose handling, serum lipid disorders, hepatic steatosis, increased weight of white adipose tissues and kidney fibrosis in HFD+L-NAME-treated mice. In the established HFD+L-NAME-induced HFpEF and metabolic syndrome mouse model, therapeutic treatment with nitazoxanide rescued HFD+L-NAME-induced pathological phenotypes as mentioned above. The in vitro experiments revealed that tizoxanide, the active metabolite of nitazoxanide, increased the basal mitochondria metabolism of cardiomyocytes, inhibited cardiomyocyte hypertrophy and collagen secretion from cardiac fibroblasts, and relaxed phenylephrine- and U46619-induced constriction of rat mesenteric arteries, indicating that the direct effect of tizoxanide might partly contribute to the protective effect of nitazoxanide against HFpEF in vivo . The present study suggests that nitazoxanide might be a potential drug for HFpEF and metabolic syndrome therapy. Nitazoxanide protects against experimental heart failure with preserved ejection (HFpEF) and metabolic syndrome in mice, suggesting that nitazoxanide might be a potential drug for HFpEF and metabolic syndrome therapy.
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Chen et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF) and metabolic syndrome. Nitazoxanide was evaluated on Cardiac hypertrophy, cardiac fibrosis, cardiac diastolic dysfunction, and metabolic syndrome phenotypes. Oral nitazoxanide improved cardiac hypertrophy, diastolic dysfunction, and metabolic syndrome phenotypes in a mouse model of HFD plus L-NAME-induced HFpEF.
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