ArticleESC heart failure2025
Vericiguat improves cardiac remodelling and function in rats with doxorubicin-induced cardiomyopathy.
Article in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Therapeutic effect of Fuzheng Yixin decoction on cardiac insufficiencythe soluble guanylyl cyclase-cyclic guanosine monophosphate-protein kinase G pathway in a doxorubicin-induced dilated cardiomyopathy rat model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Recovery of cardiac function in Desmin cardiomyopathy with medical therapy.Orphanet journal of rare diseases · 2026Article
- Vericiguat Alleviates Atrial Electrical and Structural Remodeling in Rats with Atrial Fibrillation.Anatolian journal of cardiology · 2026Article
- The emerging role of Nrf2 in heart failure: From cardioprotection to therapeutic approaches.ESC heart failure · 2025Review
- Therapeutic Impact of Vericiguat on Ventricular Remodeling in a Pressure-Overload Heart Failure Model.Life (Basel, Switzerland) · 2025Article
- Vericiguat improves cardiac remodelling and function in rats with doxorubicin-induced cardiomyopathy.ESC heart failure · 2025Article
- NO/NOS system dysregulation as a key molecular mechanism in chemotherapy-induced cardiotoxicity: a review.Frontiers in cardiovascular medicine · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
purposeVericiguat, a soluble guanylate cyclase (sGC) stimulator, has been demonstrated effective in improving prognosis of patients with heart failure with reduced ejection fraction. However, there are limited data concerning the effect of vericiguat in patients with doxorubicin (DOX)-induced cardiomyopathy (DIC). In this study, we investigated the effects of vericiguat on cardiac structure and function in rats with DIC as well as their potential mechanisms of action.
methodsDIC rats were established by intraperitoneal injection of DOX (1 mg/kg) twice a week for 6 weeks, followed by intragastric administration of vericiguat 1 mg/kg/day or an equal volume of normal saline for 8 weeks. Cardiac histology and function, circulating levels of amino-terminal pro-B-type natriuretic peptide (NT-proBNP), nitric oxide (NO), and oxidative indices, as well as myocardial cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signalling, oxidative and apoptosis-associated protein were measured.
resultsCompared with the control group, rats treated with DOX exhibited significantly increased heart size, reduced systolic function and elevated plasma levels of NT-proBNP. Histological findings revealed myocardial cell atrophy, fibrosis and apoptosis. Vericiguat treatment effectively reversed DOX-induced cardiac remodelling and improved systolic function. Mechanistically, Vericiguat attenuated the inhibitory effects of DOX on the myocardial cGMP-PKG axis and nuclear factor erythroid 2-related factor 2 (Nrf2) protein, thereby alleviating oxidative stress and apoptosis.
conclusionsVericiguat improved cardiac remodelling and contractile function in rats with DIC through upregulation of cGMP-PKG signalling and inhibition of oxidative stress and myocardial apoptosis.
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