Evidence map›Paper›PMID 27249171›Full record

ArticleNature communications2016

The ubiquitin E3 ligase TRAF6 exacerbates pathological cardiac hypertrophy via TAK1-dependent signalling.

Yan-Xiao Ji, Peng Zhang, Xiao-Jing Zhang, Yi-Chao Zhao, Ke-Qiong Deng, Xi Jiang, Pi-Xiao Wang, Zan Huang, Hongliang Li

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 181 citations in OpenAlex.

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  5. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
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27 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Yan-Xiao JiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Peng ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Xiao-Jing ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Yi-Chao ZhaoDepartment of Cardiology, Shanghai Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.
Ke-Qiong DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Xi JiangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Pi-Xiao WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Zan HuangCollege of Life Science, Wuhan University, Wuhan 430072, China.
Hongliang LiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wuhan University · CNRenmin Hospital of Wuhan University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour necrosis factor receptor-associated factor 6 (TRAF6) is a ubiquitin E3 ligase that regulates important biological processes. However, the role of TRAF6 in cardiac hypertrophy remains unknown. Here, we show that TRAF6 levels are increased in human and murine hypertrophied hearts, which is regulated by reactive oxygen species (ROS) production. Cardiac-specific Traf6 overexpression exacerbates cardiac hypertrophy in response to pressure overload or angiotensin II (Ang II) challenge, whereas Traf6 deficiency causes an alleviated hypertrophic phenotype in mice. Mechanistically, we show that ROS, generated during hypertrophic progression, triggers TRAF6 auto-ubiquitination that facilitates recruitment of TAB2 and its binding to transforming growth factor beta-activated kinase 1 (TAK1), which, in turn, enables the direct TRAF6-TAK1 interaction and promotes TAK1 ubiquitination. The binding of TRAF6 to TAK1 and the induction of TAK1 ubiquitination and activation are indispensable for TRAF6-regulated cardiac remodelling. Taken together, we define TRAF6 as an essential molecular switch leading to cardiac hypertrophy in a TAK1-dependent manner.

Indexed as

AnimalsAnimals, NewbornCardiomegalyCells, CulturedHEK293 CellsHumansMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMice, Inbred C57BLMice, KnockoutMice, TransgenicProtein BindingRats, Sprague-DawleySignal TransductionTNF Receptor-Associated Factor 6UbiquitinationMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesTNF Receptor-Associated Factor 6Ubiquitin-Protein Ligases

Identifiers

PMID27249171
PMCPMC4895385
OpenAlexW2468750744

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.