Evidence map›Paper›PMID 34907169›Full record

ArticleCell death discovery2021

TRAP1 inhibits MIC60 ubiquitination to mitigate the injury of cardiomyocytes and protect mitochondria in extracellular acidosis.

Lingxiao Zhang, Ning Su, Yuanyuan Luo, Siyin Chen, Tongfeng Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Lingxiao Zhang *Departments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.ORCID http://orcid.org/0000-0001-5196-9653
Ning Su *Departments of Nephrology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
Yuanyuan LuoDepartments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
Siyin ChenDepartments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
Tongfeng ZhaoDepartments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China. zhaotf@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-5293-0670
Sun Yat-sen University · CN

Funding

Guangzhou Science and Technology Program key projects 201604020119
6 · The paper itself

Abstract

Extracellular acidosis-induced mitochondrial damage of cardiomyocytes leads to cardiac dysfunction, but no detailed mechanism or efficient therapeutic target has been reported. Here we found that the protein levels of MIC60 were decreased in H9C2 cells and heart tissues in extracellular acidosis, which caused mitochondrial damage and cardiac dysfunction. Overexpression of MIC60 maintains H9C2 cells viability, increases ATP production and mitochondrial membrane potential, mitigates the disruptions of mitochondrial structure and cardiac injury. Mechanistically, extracellular acidosis excessively promoted MIC60 ubiquitin-dependent degradation. TRAP1 mitigated acidosis-induced mitochondrial impairments and cardiac injury by directly interacting with MIC60 to decrease its ubiquitin-dependent degradation in extracellular acidosis.

Identifiers

PMID34907169
PMCPMC8671480
OpenAlexW4200344072

What OpenQuestion 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 OpenQuestion graph.