Evidence map›Paper›PMID 39729180›Full record

ArticleCardiovascular toxicology2025

SUZ12-Increased NRF2 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Apoptosis, Inflammation, and Ferroptosis.

Guoyong Zhang, Zhimin Ma, Zheng Ma, Peilin Liu, Lin Zhang, Zheng Lian, Caixia Guo

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Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

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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

4 citing papers in PubMed.

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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

7 authors.

Guoyong Zhang *Department of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Zhimin Ma *Department of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Zheng MaDepartment of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Peilin LiuDepartment of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Lin ZhangDepartment of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Zheng LianDepartment of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China.
Caixia GuoDepartment of Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, No. 3 Chongwenmennei Street, Dongcheng District, Beijing, 100730, China. g1c9x76@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury. qRT-PCR and western blot assays were used to detect the levels of mRNAs and proteins. Cardiomyocyte injury was determined by detecting the levels of lactate dehydrogenase and creatine Kinase MB (CK-MB). Cell apoptosis was investigated by flow cytometry and related markers. Levels of IL-6, IL-10, and TNF-α were measured by ELISA. Cell ferroptosis was assessed by detecting the production of reactive oxygen species (ROS), malonaldehyde (MDA), reduced glutathione/oxidized glutathione disulfide (GSH/GSSG) ratio, Fe + content, and related regulators. The interaction between NRF2 and the suppressor of zest 12 (SUZ12) was analyzed by using dual-luciferase reporter and RNA immunoprecipitation assays. AMI rat models were established for in vivo analysis. NRF2 was lowly expressed in AMI patients and H/R-induced cardiomyocytes. Forced expression of NRF2 reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis. Moreover, NRF2 overexpression improved cardiac function and injury in vivo. Mechanistically, SUZ12 bound to the promoter of NRF2 and promoted its expression. Further functional analyses showed that SUZ12 overexpression reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis, which were reversed by NRF2 silencing. SUZ12-increased NRF2 suppressed H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis in vitro and improved cardiac functions in rats with I/R injury, suggesting the potential cardioprotective effect of NRF2 in cardiac injury during AMI.

Indexed as

ApoptosisFerroptosisInflammationInflammation MediatorsMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNF-E2-Related Factor 2AnimalsCells, CulturedCytokinesDisease Models, AnimalHumansMaleRats, Sprague-DawleySignal TransductionCytokinesInflammation MediatorsNFE2L2 protein, humanNfe2l2 protein, ratNF-E2-Related Factor 2ApoptosisFerroptosisInflammationMyocardial ischemiaNRF2SUZ12

Identifiers

PMID39729180

What Socratic holds

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Registered trials

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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.