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An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)

  • Authors:
    • Sirun Qin
    • Can Zhu
    • Chenyang Chen
    • Zhe Sheng
    • Yu Cao
  • View Affiliations / Copyright

    Affiliations: Department of Cardiovascular Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of Cardiovascular Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China
    Copyright: © Qin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 16
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    Published online on: November 11, 2024
       https://doi.org/10.3892/ijmm.2024.5457
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Abstract

The pathophysiology of cardiovascular disease (CVD) is complex and presents a serious threat to human health. Cardiomyocyte loss serves a pivotal role in both the onset and progression of CVD. Among various forms of programmed cell death, ferroptosis, along with apoptosis, autophagy and pyroptosis, is closely linked to the advancement of CVD. Ferroptosis, a mechanism of cell death, is driven by the buildup of oxidized lipids and excess iron. This pathway is modulated by lipid, amino acid and iron metabolism. Key characteristics of ferroptosis include disrupted iron homeostasis, increased peroxidation of polyunsaturated fatty acids due to reactive oxygen species, decreased glutathione levels and inactivation of glutathione peroxidase 4. Treatments targeting ferroptosis could potentially prevent or alleviate CVD by inhibiting the ferroptosis pathway. Ferroptosis is integral to the pathogenesis of several types of CVD and inhibiting its occurrence in cardiomyocytes could be a promising therapeutic strategy for the future treatment of CVD. The present review provided an in‑depth analysis of advancements in understanding the mechanisms underlying ferroptosis. The present manuscript summarized the interplay between ferroptosis and CVDs, highlighting its dual roles in these conditions. Additionally, potential therapeutic targets within the ferroptosis pathway were discussed, alongside the current limitations and future directions of these novel treatment strategies. The present review may offer novel insights into preventive and therapeutic approaches for CVDs.
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Spandidos Publications style
Qin S, Zhu C, Chen C, Sheng Z and Cao Y: An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review). Int J Mol Med 55: 16, 2025.
APA
Qin, S., Zhu, C., Chen, C., Sheng, Z., & Cao, Y. (2025). An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review). International Journal of Molecular Medicine, 55, 16. https://doi.org/10.3892/ijmm.2024.5457
MLA
Qin, S., Zhu, C., Chen, C., Sheng, Z., Cao, Y."An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)". International Journal of Molecular Medicine 55.1 (2025): 16.
Chicago
Qin, S., Zhu, C., Chen, C., Sheng, Z., Cao, Y."An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)". International Journal of Molecular Medicine 55, no. 1 (2025): 16. https://doi.org/10.3892/ijmm.2024.5457
Copy and paste a formatted citation
x
Spandidos Publications style
Qin S, Zhu C, Chen C, Sheng Z and Cao Y: An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review). Int J Mol Med 55: 16, 2025.
APA
Qin, S., Zhu, C., Chen, C., Sheng, Z., & Cao, Y. (2025). An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review). International Journal of Molecular Medicine, 55, 16. https://doi.org/10.3892/ijmm.2024.5457
MLA
Qin, S., Zhu, C., Chen, C., Sheng, Z., Cao, Y."An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)". International Journal of Molecular Medicine 55.1 (2025): 16.
Chicago
Qin, S., Zhu, C., Chen, C., Sheng, Z., Cao, Y."An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)". International Journal of Molecular Medicine 55, no. 1 (2025): 16. https://doi.org/10.3892/ijmm.2024.5457
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