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Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review)

  • Authors:
    • Liang Han
    • Wen Zhai
  • View Affiliations / Copyright

    Affiliations: Center for Rehabilitation Medicine, Department of Anesthesiology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang 310014, P.R. China
    Copyright: © Han et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 105
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    Published online on: February 21, 2025
       https://doi.org/10.3892/mmr.2025.13470
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Abstract

Ischemia‑reperfusion injury (IRI) refers to tissue or organ damage that occurs following a period of inadequate blood supply (ischemia) followed by restoration of blood flow (reperfusion) within a short time frame. This phenomenon is prevalent in clinical conditions such as cardiovascular and cerebrovascular disease, organ transplantation and stroke. Despite its frequency, effective therapeutic strategies to mitigate IRI remain elusive in clinical practice, underscoring the need for a deeper understanding of its molecular mechanisms. Aldehyde dehydrogenase 2 (ALDH2), a key enzyme in alcohol metabolism, serves a role in alleviating oxidative stress and cell damage during IRI by modulating oxidative stress, decreasing apoptosis and inhibiting inflammatory responses. ALDH2 exerts protective effects by detoxifying reactive aldehydes, thereby preventing lipid peroxidation and maintaining cellular homeostasis. Furthermore, ferroptosis, a regulated form of cell death driven by iron accumulation and subsequent lipid peroxidation, is a key process in IRI. However, the precise role of ALDH2 in modulating ferroptosis during IRI remains incompletely understood. Although there is an interaction between ALDH2 activity and ferroptosis, the underlying mechanisms have yet to be clarified. The present review examines the role of ALDH2 and ferroptosis in IRI and the potential regulatory influence of ALDH2 on ferroptosis mechanisms, as well as potential targeting of ALDH2 and ferroptosis for IRI treatment and prevention. By elucidating the complex interplay between ALDH2 and ferroptosis, the present review aims to provide new insights for the development of innovative therapeutic strategies to mitigate ischemic tissue damage and improve clinical outcomes.
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Copy and paste a formatted citation
Spandidos Publications style
Han L and Zhai W: Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review). Mol Med Rep 31: 105, 2025.
APA
Han, L., & Zhai, W. (2025). Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review). Molecular Medicine Reports, 31, 105. https://doi.org/10.3892/mmr.2025.13470
MLA
Han, L., Zhai, W."Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review)". Molecular Medicine Reports 31.4 (2025): 105.
Chicago
Han, L., Zhai, W."Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review)". Molecular Medicine Reports 31, no. 4 (2025): 105. https://doi.org/10.3892/mmr.2025.13470
Copy and paste a formatted citation
x
Spandidos Publications style
Han L and Zhai W: Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review). Mol Med Rep 31: 105, 2025.
APA
Han, L., & Zhai, W. (2025). Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review). Molecular Medicine Reports, 31, 105. https://doi.org/10.3892/mmr.2025.13470
MLA
Han, L., Zhai, W."Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review)". Molecular Medicine Reports 31.4 (2025): 105.
Chicago
Han, L., Zhai, W."Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review)". Molecular Medicine Reports 31, no. 4 (2025): 105. https://doi.org/10.3892/mmr.2025.13470
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