ArticlePloS one2025
Dapagliflozin inhibits ferroptosis to improve chronic heart failure by regulating Nrf2/HO-1/GPX4 signaling pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Dapagliflozin Protects Cardiomyocytes against Doxorubicin-Induced Toxicity by Modulating Sirtuin 1/Sirtuin 3 and Ferroptosis Pathway.ACS pharmacology & translational science · 2026Article
- Beyond glycemic control: SGLT2 inhibitors as time-sensitive organ-protective agents in acute injury-mechanistic insights and translational implications.Frontiers in pharmacology · 2026Review
- Bibliometric and visual analysis of ferroptosis in cardiovascular diseases.Journal of cardiothoracic surgery · 2025Review
- Sodium-glucose cotransporter 2 inhibitors ameliorate glutathione cysteine ligase modifier-mediated oxidative stress and subsequent ferroptosis in proximal tubules of diabetic kidney disease.Redox report : communications in free radical research · 2025Article
- The emerging role of Nrf2 in heart failure: From cardioprotection to therapeutic approaches.ESC heart failure · 2025Review
- Review
- The Nrf Family and Its Cardioprotective Potential: Mechanisms, Functions, and Therapeutic Perspectives.Drug design, development and therapy · 2025Review
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveTo study the effect of Dapagliflozin on ferroptosis in rabbits with chronic heart failure and to reveal its possible mechanism.
methodsNine healthy adult male New Zealand white rabbits were randomly divided into Sham group (only thorax opening was performed in Sham group, no ascending aorta circumferential ligation was performed), Heart failure group (HF group, ascending aorta circumferential ligation was performed in HF group to establish the animal model of heart failure), and Dapagliflozin group (DAPA group, after the rabbit chronic heart failure model was successfully made in DAPA group). Dapagliflozin was given by force-feeding method. Echocardiography was used to assess cardiac function, HE staining to evaluate pathological changes in the heart, Prussia blue staining to observe iron ions in myocardial tissue, and enzyme-linked immunosorbent assay (ELISA) to determine serum levels of the inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) at the end of week 12 and/or the end of week 16. The oxidative stress related indexes of malondialdehyde (MDA), superoxide dismutase (SOD) and superoxide dismutase (GSH-Px) in serum were quantitatively analyzed by colorimetry. Protein expression levels of nuclear factor E2-related factor 2(Nrf2), heme oxygenase-1(HO-1), glutathione peroxidase 4(Gpx4) were detected by Western blot.
resultsIn animals with chronic heart failure, Dapagliflozin improved cardiomyocyte hypertrophy, degeneration and necrosis. Dapagliflozin increased serum GSH-Px and SOD levels and decreased IL-1β, IL-6, TNF-α and MDA levels (P < 0.05) in a rabbit model of heart failure. Dapagliflozin also decreased cardiac iron ion levels and increased Nrf2, HO-1 and GPX4 protein expression.
conclusionDapagliflozin can improve heart failure by inhibiting oxidative stress and ferroptosis, and its mechanism may be related to the regulation of Nrf2/HO-1/GPX4 signaling pathway.
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