Evidence map›Paper›PMID 38852121›Full record

ReviewMolecular biotechnology2025

Management of ROS and Regulatory Cell Death in Myocardial Ischemia-Reperfusion Injury.

Ge Gong, Wenhui Wan, Xinghu Zhang, Xiangxuan Chen, Jian Yin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  12. 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

5 authors.

Ge Gong *Department of Geriatrics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 211002, China.
Wenhui Wan *Department of Geriatrics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 211002, China.
Xinghu ZhangDepartment of Geriatrics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 211002, China.
Xiangxuan ChenDepartment of Cardiology, the Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, 211100, China. cxxjnyy@163.com.
Jian YinDepartment of Orthopedics, the Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, 211100, China. yinjiandoc@163.com.ORCID http://orcid.org/0000-0002-6435-775X

Funding

Applied research project unit of geriatric medicine clinical technology in Jiangsu Province LD2022001Jiangsu Medical Vocational College Clinical Teaching Base Special Scientific Research Development Fund 20229103Management project of Jinling Hospital Affiliated to Nanjing University YYQN2021097Nanjing Health Science and Technology Development Special Fund Project YKK22222Nanjing Medical University Kangda College Scientific Research Development Fund Project KD2023KYJJ230
6 · The paper itself

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is fatal to patients, leading to cardiomyocyte death and myocardial remodeling. Reactive oxygen species (ROS) and oxidative stress play important roles in MIRI. There is a complex crosstalk between ROS and regulatory cell deaths (RCD) in cardiomyocytes, such as apoptosis, pyroptosis, autophagy, and ferroptosis. ROS is a double-edged sword. A reasonable level of ROS maintains the normal physiological activity of myocardial cells. However, during myocardial ischemia-reperfusion, excessive ROS generation accelerates myocardial damage through a variety of biological pathways. ROS regulates cardiomyocyte RCD through various molecular mechanisms. Targeting the removal of excess ROS has been considered an effective way to reverse myocardial damage. Many studies have applied antioxidant drugs or new advanced materials to reduce ROS levels to alleviate MIRI. Although the road from laboratory to clinic has been difficult, many scholars still persevere. This article reviews the molecular mechanisms of ROS inhibition to regulate cardiomyocyte RCD, with a view to providing new insights into prevention and treatment strategies for MIRI.

Indexed as

Myocardial Reperfusion InjuryReactive Oxygen SpeciesAnimalsAntioxidantsApoptosisAutophagyCell DeathFerroptosisHumansMyocytes, CardiacOxidative StressAntioxidantsReactive Oxygen SpeciesMyocardial ischemia–reperfusion injuryNrf2Oxidative stressRegulated cell deathROS

Identifiers

PMID38852121

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.