Evidence map›Paper›PMID 32343488›Full record

ArticleJournal of cellular and molecular medicine2020

Tripartite motif 10 regulates cardiac hypertrophy by targeting the PTEN/AKT pathway.

Hui Yang, Xiao-Xiao Wang, Chun-Yu Zhou, Xue Xiao, Cui Tian, Hui-Hua Li, Chun-Lin Yin, Hong-Xia Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

  • Erratum issued
    .2023
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Hui YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xiao-Xiao WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Chun-Yu ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xue XiaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Cui TianDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Hui-Hua LiDepartment of Cardiology, Institute of Cardiovascular Diseases, First Affiliated hospital of Dalian Medical University, Dalian, China.
Chun-Lin YinDepartment of Cardiology, Xuan Wu Hospital, Capital Medical University, Beijing, China.
Hong-Xia WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.ORCID 0000-0003-4876-2138
Capital Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of cardiac hypertrophy is tightly associated with activation of intracellular hypertrophic signalling pathways, which leads to the synthesis of various proteins. Tripartite motif 10 (TRIM10) is an E3 ligase with important functions in protein quality control. However, its role in cardiac hypertrophy was unclear. In this study, neonatal rat cardiomyocytes (NRCMs) and TRIM10-knockout mice were subjected to phenylephrine (PE) stimulation or transverse aortic constriction (TAC) to induce cardiac hypertrophy in vitro and in vivo, respectively. Trim10 expression was significantly increased in hypertrophied murine hearts and PE-stimulated NRCMs. Knockdown of TRIM10 in NRCMs alleviated PE-induced changes in the size of cardiomyocytes and hypertrophy gene expression, whereas TRIM10 overexpression aggravated these changes. These results were further verified in TRIM10-knockout mice. Mechanistically, we found that TRIM10 knockout or knockdown decreased AKT phosphorylation. Furthermore, we found that TRIM10 knockout or knockdown increased ubiquitination of phosphatase and tensin homolog (PTEN), which negatively regulated AKT activation. The results of this study reveal the involvement of TRIM10 in pathological cardiac hypertrophy, which may occur by prompting of PTEN ubiquitination and subsequent activation of AKT signalling. Therefore, TRIM10 may be a promising target for treatment of cardiac hypertrophy.

Indexed as

Signal TransductionAnimalsAortaCardiomegalyConstriction, PathologicIntracellular Signaling Peptides and ProteinsMice, Inbred C57BLMice, KnockoutPhosphorylationProteolysisProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRatsRats, Sprague-DawleySTAT3 Transcription FactorTripartite Motif ProteinsIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSTAT3 Transcription FactorTRIM10 protein, mouseTrim10 protein, ratTripartite Motif ProteinsAKTCardiac hypertrophyPTENTransverse aortic constrictionTRIM10

Identifiers

PMID32343488
PMCPMC7294125
OpenAlexW3018203587

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.