Evidence map›Paper›PMID 39247823›Full record

ArticleInternational journal of biological sciences2024

Nuclear receptor subfamily 4 group A member 1 promotes myocardial ischemia/reperfusion injury through inducing mitochondrial fission factor-mediated mitochondrial fragmentation and inhibiting FUN14 domain containing 1-depedent mitophagy.

Junyan Wang, Haowen Zhuang, Lianqun Jia, Xinyong He, Sicheng Zheng, Kangshou Ji, Kang Xie, Tong Ying, Ying Zhang, Chun Li and 1 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

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

  1. Pooled it
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  9. Raptor and Drp1 Function Synthetically to Control Hypoxic Death and the Mitochondrial Network in Caenorhabditis elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  19. Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026
    Review
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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

11 authors.

Junyan WangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Haowen ZhuangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Lianqun JiaLiaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110032, China.
Xinyong HeLiaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110032, China.
Sicheng ZhengLiaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110032, China.
Kangshou JiLiaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110032, China.
Kang XieSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Tong YingLiaoning University of Traditional Chinese Medicine, Shenyang, Liaoning, 110032, China.
Ying ZhangSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing 100048 Beijing, China.
Chun LiSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Xing ChangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study investigated the mechanism by which NR4A1 regulates mitochondrial fission factor (Mff)-related mitochondrial fission and FUN14 domain 1 (FUNDC1)-mediated mitophagy following cardiac ischemia-reperfusion injury(I/R). Our findings showed that the damage regulation was positively correlated with the pathological fission and pan-apoptosis of myocardial cell mitochondria. Compared with wild-type mice (WT), NR4A1-knockout mice exhibited resistance to myocardial ischemia-reperfusion injury and mitochondrial pathological fission, characterized by mitophagy activation. Results showed that ischemia-reperfusion injury increased NR4A1 expression level, activating mitochondrial fission mediated by Mff and restoring the mitophagy phenotype mediated by FUNDC1. The inactivation of FUNDC1 phosphorylation could not mediate the normalization of mitophagy in a timely manner, leading to an excessive stress response of unfolded mitochondrial proteins and an imbalance in mitochondrial homeostasis. This process disrupted the normalization of the mitochondrial quality control network, leading to accumulation of damaged mitochondria and the activation of pan-apoptotic programs. Our data indicate that NR4A1 is a novel and critical target in myocardial I/R injury that exertsand negative regulatory effects by activating Mff-mediated mito-fission and inhibiting FUNDC1-mediated mitophagy. Targeting the crosstalk balance between NR4A1-Mff-FUNDC1 is a potential approach for treating I/R.

Indexed as

Mice, KnockoutMitochondrial DynamicsMitochondrial ProteinsMitophagyMyocardial Reperfusion InjuryNuclear Receptor Subfamily 4, Group A, Member 1AnimalsApoptosisMaleMembrane ProteinsMiceMice, Inbred C57BLMitochondriaMitochondria, HeartFUNDC1 protein, mouseMembrane Proteinsmitochondrial fission factor, mouseMitochondrial ProteinsNr4a1 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 1FUNDC1Mffmyocardial ischemia-reperfusion injuryNR4A1pan-apoptosis

Identifiers

PMID39247823
PMCPMC11380451

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.