Evidence map›Paper›PMID 40447880›Full record

ArticleCell biology and toxicology2025

cIAP2-mediated IGF2BP2 ubiquitination and degradation regulate cardiomyocyte apoptosis via stabilizing m

Cong Wang, Jijia Liu, Xuyang Hou, Qing Guan, Huiling Zhou, Yong Luo, Wancun Jin, Fan Bai, Lijun Liu, Jian Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Cong Wang *Department of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Jijia Liu *Department of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xuyang HouDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Qing GuanDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Huiling ZhouDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yong LuoDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Wancun JinDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Fan BaiDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Lijun LiuDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Jian WangDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Li XieDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Feng LiDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Haidan LiuDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China. haidanliu@csu.edu.cn.

Funding

National Natural Science Foundation of China 82073260Natural Science Foundation of Hunan Province 2023JJ30766
6 · The paper itself

Abstract

Ubiquitin-proteasome system (UPS) is a major degradation system that maintains cardiac proteostasis, thus displaying an indispensable role in coronary artery disease, including myocardial infarction (MI). However, the function and mechanism of ubiquitin ligases in MI remain unclarified. In this study, we reported that cIAP2 protein, an E3 ubiquitin ligase, was downregulated in MI tissue and oxygen-glucose deprivation (OGD)-treated cardiomyocytes (CMs). cIAP2 depletion promoted OGD-induced injury and apoptosis in CMs, while adeno-associated virus (AAV) serotype 9 mediated-cardiac specific cIAP2 overexpression inhibited myocardial injury in MI mice. Moreover, we identified IGF2BP2 as a novel substrate of cIAP2. Mechanistically, cIAP2 downregulation inhibited IGF2BP2 ubiquitination and proteasomal degradation, leading to the upregulation of IGF2BP2 protein, which subsequently enhanced OGD-induced injury and apoptosis by stabilizing BAX mRNA in an m

Indexed as

Apoptosisbcl-2-Associated X ProteinInhibitor of Apoptosis ProteinsMyocardial InfarctionMyocytes, CardiacRNA-Binding ProteinsUbiquitin-Protein LigasesAnimalsGlucoseHumansMaleMiceMice, Inbred C57BLProteolysisRNA, MessengerUbiquitinationbcl-2-Associated X ProteinGlucoseInhibitor of Apoptosis ProteinsRNA-Binding ProteinsRNA, MessengerUbiquitin-Protein LigasesApoptosisCIAP2IGF2BP2Myocardial infarctionN6-methyladenosineUbiquitination

Identifiers

PMID40447880
PMCPMC12125055

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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 OpenQuestion graph.