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Cited by 448

The DOI matches its Crossref record; 115 of the 115 references it cites were found in a registry or an index.

Regulated cell death in myocardial ischemia–reperfusion injury

Xiang, Qi, Yi, Xin, Zhu, Xue-Hai, Wei, Xiang, Jiang, Ding-Sheng·2024·Trends in Endocrinology & Metabolism

Abstract

Myocardial ischemia-reperfusion (I/R) injury most commonly occurs in coronary artery disease when prompt reperfusion is used to salvage the ischemic myocardium. Cardiomyocyte death is a significant component of myocardial I/R injury and its mechanism was previously thought to be limited to apoptosis and necrosis. With the discovery of novel types of cell death, ferroptosis, necroptosis, and pyroptosis have been shown to be involved in myocardial I/R. These new forms of regulated cell death cause cardiomyocyte loss and exacerbate I/R injury by affecting reactive oxygen species (ROS) generation, calcium stress, and inflammatory cascades, subsequently mediating adverse remodeling, cardiac dysfunction, and heart failure. Herein, we review the roles of ferroptosis, necroptosis, and pyroptosis in myocardial I/R and discuss their contribution to pathology.

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Crossref · 10.1016/j.tem.2023.10.010

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Metadata

Authors
Xiang, Q., Yi, X., Zhu, X.-H., Wei, X., & Jiang, D.-S.
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2024-03
Volume
35
Issue
3
Pages
219-234
ISSN
1043-2760 (ISSN-L)
OpenAlex
W4388776088
Cited by
448
References
115
FWCI
32.01
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Regulated cell death in myocardial ischemia–reperfusion injury. https://app.cochat.ai/papers/10.1016/j.tem.2023.10.010
The paper
Xiang, Q., Yi, X., Zhu, X.-H., Wei, X., & Jiang, D.-S. (2024). Regulated cell death in myocardial ischemia–reperfusion injury. Trends in Endocrinology & Metabolism. https://doi.org/10.1016/j.tem.2023.10.010

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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