Evidence map›Paper›PMID 40044643›Full record

ReviewCell death discovery2025

Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.

Bingxin Du, Qiang Fu, Qin Yang, Yeying Yang, Rui Li, Xu Yang, Qingrong Yang, Shuo Li, Jinwei Tian, Huibin Liu

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  15. ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Bingxin Du *Department of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Qiang Fu *Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, Harbin, China.
Qin Yang *Department of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yeying YangDepartment of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Rui LiDepartment of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xu YangDepartment of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Qingrong YangDepartment of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shuo LiHeilongjiang Provincial Key Laboratory of Panvascular Disease, Harbin, China.
Jinwei TianHeilongjiang Provincial Key Laboratory of Panvascular Disease, Harbin, China. tianjinwei@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-2730-0033
Huibin LiuDepartment of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China. liuhuibin@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-9535-3719

Funding

Natural Science Foundation of Heilongjiang Province PL2024H080Natural Science Foundation of Heilongjiang Province ZD2023H005
6 · The paper itself

Abstract

Myocardial ischemia-reperfusion (I/R) injury is a multifaceted process observed in patients with coronary artery disease when blood flow is restored to the heart tissue following ischemia-induced damage. Cardiomyocyte cell death, particularly through apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis, is pivotal in myocardial I/R injury. Preventing cell death during the process of I/R is vital for improving ischemic cardiomyopathy. These multiple forms of cell death can occur simultaneously, interact with each other, and contribute to the complexity of myocardial I/R injury. In this review, we aim to provide a comprehensive summary of the key molecular mechanisms and regulatory patterns involved in these five types of cell death in myocardial I/R injury. We will also discuss the crosstalk and intricate interactions among these mechanisms, highlighting the interplay between different types of cell death. Furthermore, we will explore specific molecules or targets that participate in different cell death pathways and elucidate their mechanisms of action. It is important to note that manipulating the molecules or targets involved in distinct cell death processes may have a significant impact on reducing myocardial I/R injury. By enhancing researchers' understanding of the mechanisms and interactions among different types of cell death in myocardial I/R injury, this review aims to pave the way for the development of novel interventions for cardio-protection in patients affected by myocardial I/R injury.

Identifiers

PMID40044643
PMCPMC11883039

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.