Evidence map›Paper›PMID 29971943›Full record

ArticleJournal of cellular and molecular medicine2018

TWEAK/Fn14 mediates atrial-derived HL-1 myocytes hypertrophy via JAK2/STAT3 signalling pathway.

Li Hao, Manyi Ren, Bing Rong, Fei Xie, Ming-Jie Lin, Ya-Chao Zhao, Xin Yue, Wen-Qiang Han, Jing-Quan Zhong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 27 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

9 authors at 1 institution in 1 country.

Li HaoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.ORCID 0000-0003-1928-304X
Manyi RenThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Bing RongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Fei XieThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Ming-Jie LinThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Ya-Chao ZhaoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Xin YueThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Wen-Qiang HanThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Jing-Quan ZhongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial myocyte hypertrophy is one of the most important substrates in the development of atrial fibrillation (AF). The TWEAK/Fn14 axis is a positive regulator of cardiac hypertrophy in cardiomyopathy. This study therefore investigated the effects of Fn14 on atrial hypertrophy and underlying cellular mechanisms using HL-1 atrial myocytes. In patients with AF, Fn14 protein levels were higher in atrial myocytes from atrial appendages, and expression of TWEAK was increased in peripheral blood mononuclear cells, while TWEAK serum levels were decreased. In vitro, Fn14 expression was up-regulated in response to TWEAK treatment in HL-1 atrial myocytes. TWEAK increased the expression of ANP and Troponin T, and Fn14 knockdown counteracted the effect. Inhibition of JAK2, STAT3 by specific siRNA attenuated TWEAK-induced HL-1 atrial myocytes hypertrophy. In conclusion, TWEAK/Fn14 axis mediates HL-1 atrial myocytes hypertrophy partly through activation of the JAK2/STAT3 pathway.

Indexed as

AgedAnimalsAtrial FibrillationAtrial Natriuretic FactorCardiomegalyCase-Control StudiesCytokine TWEAKDisease Models, AnimalFemaleGene Expression RegulationHeart AtriaHumansJanus Kinase 2Leukocytes, MononuclearMaleMiceAtrial Natriuretic FactorCytokine TWEAKJak2 protein, mouseJanus Kinase 2RNA, Small InterferingStat3 protein, mouseSTAT3 Transcription FactorTnfrsf12a protein, mouseTnfsf12 protein, mouseTroponin TTWEAK ReceptorFn14HL-1 atrial myocyteshypertrophyJAK2/STAT3TWEAK

Identifiers

PMID29971943
PMCPMC6111870
OpenAlexW2810900592

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.