Evidence map›Paper›PMID 27815660›Full record

ArticleIn vitro cellular & developmental biology. Animal2017

Mitochondrial phosphatase PGAM5 regulates Keap1-mediated Bcl-xL degradation and controls cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury.

Chen Yang, Xiaojuan Liu, Fangfang Yang, Weixun Zhang, Zihao Chen, Daliang Yan, Qingsheng You, Xiang Wu

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025
    Review
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  7. 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

8 authors at 2 institutions in 1 country.

Chen YangDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Xiaojuan LiuDepartment of Pathogen Biology, Medical College, Nantong University, Nantong, Jiangsu, 226001, China.
Fangfang YangDepartment of Infection Diseases, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Weixun ZhangMedical College, Nantong University, Nantong, Jiangsu, 226001, China.
Zihao ChenDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Daliang YanDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Qingsheng YouDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China. youqs_pro001@sina.com.
Xiang WuDepartment of Vasculocardiology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China. ntwx0513@163.com.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoglycerate mutase 5 (PGAM5) is a mitochondrial membrane protein that plays crucial roles in necroptosis and apoptosis. Though PGAM5 is known to be required for inducing intrinsic apoptosis through interacting with BCL2 associated X protein (Bax) and dynamin-related protein 1 (Drp1), the expression and role of PGAM5 in cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury(MIRI) has not been studied. The present study shows that PGAM5 expression decreased after MIRI in vivo, positively correlated with Bcl-xL expression, negatively correlated with Kelch-ECH associating protein 1 (Keap1) expression. Furthermore, PGAM5 expression also decreased in cardiomyocytes after hypoxia/reoxygenation (H/R) treatment in vitro. PGAM5 silence promoted cardiomyocyte apoptosis and inhibited Bcl-xL expression, but with no effect on Keap1 expression. Accordingly, Keap1 overexpression further inhibited Bcl-xL and PGAM5 expression. Additionally, PGAM5-Bcl-xL-Keap1 interaction was identified, suggesting that PGAM5 might participate in the degradation of Bcl-xL mediated by Keap1. In summary, PGAM5 controls cardiomyocyte apoptosis induced by MIRI through regulating Keap1-mediated Bcl-xL degradation, which may supply a novel molecular target for acute myocardial infarction (AMI) therapy. Graphical abstract ᅟ.

Indexed as

AnimalsApoptosisbcl-X ProteinDisease Models, AnimalDynaminsHumansKelch-Like ECH-Associated Protein 1MitochondriaMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNecrosisPhosphoprotein PhosphatasesRatsBcl2l1 protein, ratbcl-X ProteinDnm1l protein, ratDynaminsKEAP1 protein, ratKelch-Like ECH-Associated Protein 1Phosphoprotein PhosphatasesApoptosisBcl-xLKeap1Myocardial ischemia/reperfusionPGAM5

Identifiers

PMID27815660
OpenAlexW2546420064

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.