Evidence map›Paper›PMID 38882047›Full record

ReviewDrug design, development and therapy2024

MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction.

Xiaoqing Peng, Yuanyuan Yang, Ruirui Hou, Longbiao Zhang, Can Shen, Xiaoyan Yang, Zhigang Luo, Zongzhi Yin, Yunxia Cao

Abstract readReview
In one paragraph

Review in Drug design, development and therapy, 2024. 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
–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

14 citing papers in PubMed.

  1. Article
  2. Endothelial Matrin-3 Limits Cellular Senescence and Lipid Dysregulation to Protect Against Murine Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Review
  4. Article
  5. Structural evolution of the MTCH family of mitochondrial insertases.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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.

Xiaoqing Peng *School of Pharmacy, Anhui Medical University, Hefei, People's Republic of China.ORCID 0000-0002-1958-9623
Yuanyuan Yang *Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Ruirui HouSchool of Pharmacy, Anhui Medical University, Hefei, People's Republic of China.
Longbiao ZhangSchool of Pharmacy, Anhui Medical University, Hefei, People's Republic of China.
Can ShenDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Xiaoyan YangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Zhigang LuoDepartment of Cardiology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Zongzhi YinDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.ORCID 0000-0001-5968-6332
Yunxia CaoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial carrier homolog 2 (MTCH2) is a member of the solute carrier 25 family, located on the outer mitochondrial membrane. MTCH2 was first identified in 2000. The development in MTCH2 research is rapidly increasing. The most well-known role of MTCH2 is linking to the pro-apoptosis BID to facilitate mitochondrial apoptosis. Genetic variants in MTCH2 have been investigated for their association with metabolic and neurodegenerative diseases, however, no intervention or therapeutic suggestions were provided. Recent studies revealed the physiological and pathological function of MTCH2 in metabolic diseases, neurodegenerative diseases, cancers, embryonic development and reproduction via regulating mitochondrial apoptosis, metabolic shift between glycolysis and oxidative phosphorylation, mitochondrial fusion/fission, epithelial-mesenchymal transition, etc. This review endeavors to assess a total of 131 published articles to summarise the structure and physiological/pathological role of MTCH2, which has not previously been conducted. This review concludes that MTCH2 plays a crucial role in metabolic diseases, neurodegenerative diseases, cancers, embryonic development and reproduction, and the predominant molecular mechanism is regulation of mitochondrial function. This review gives a comprehensive state of current knowledgement on MTCH2, which will promote the therapeutic research of MTCH2.

Indexed as

Embryonic DevelopmentMetabolic DiseasesNeoplasmsNeurodegenerative DiseasesReproductionAnimalsHumansMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Membrane Transport ProteinsapoptosisBIDMimpmitochondrial carrier homolog 2MTCH2

Identifiers

PMID38882047
PMCPMC11180440

What OpenQuestion holds

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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.