Evidence map›Paper›PMID 36923943›Full record

ArticleInternational journal of biological sciences2023

Transmembrane BAX inhibitor motif containing 6 suppresses presenilin-2 to preserve mitochondrial integrity after myocardial ischemia-reperfusion injury.

Li Ma, Lihan Liao, Na Zhou, Huikang Tao, Hao Zhou, Ying Tan, Weidan Chen, Fan Cao, Xinxin Chen

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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

9 authors at 2 institutions in 1 country.

Li MaGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Lihan LiaoGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Na ZhouGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Huikang TaoGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Hao ZhouDepartment of Cardiology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, 100037, China.
Ying TanDepartment of Cardiology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, 100037, China.
Weidan ChenGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Fan CaoGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Xinxin ChenGuangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Guangzhou Medical University · CNChinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia-reperfusion (I/R) damage is characterized by mitochondrial damage in cardiomyocytes. Transmembrane BAX inhibitor motif containing 6 (TMBIM6) and presenilin-2 (PS2) participate in multiple mitochondrial pathways; thus, we investigated the impact of these proteins on mitochondrial homeostasis during an acute reperfusion injury. Myocardial post-ischemic reperfusion stress impaired myocardial function, induced structural abnormalities and promoted cardiomyocyte death by disrupting the mitochondrial integrity in wild-type mice, but not in TMBIM6 transgenic mice. We found that TMBIM6 bound directly to PS2 and promoted its post-transcriptional degradation. Knocking out PS2 in mice reduced I/R injury-induced cardiac dysfunction, inflammatory responses, myocardial swelling and cardiomyocyte death by improving the mitochondrial integrity. These findings demonstrate that sufficient TMBIM6 expression can prevent PS2 accumulation during cardiac I/R injury, thus suppressing reperfusion-induced mitochondrial damage. Therefore, TMBIM6 and PS2 are promising therapeutic targets for the treatment of cardiac reperfusion damage.

Indexed as

Myocardial Reperfusion InjuryAnimalsbcl-2-Associated X ProteinMembrane ProteinsMiceMitochondriaMyocytes, CardiacPresenilin-2bcl-2-Associated X ProteinMembrane ProteinsPresenilin-2Tmbim6 protein, mousecardiac ischemia/reperfusion injurymitochondriaPS2TMBIM6

Identifiers

PMID36923943
PMCPMC10008687
OpenAlexW4324009132

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read29
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.