Evidence map›Paper›PMID 30443176›Full record

ArticleInternational journal of medical sciences2018

Tumorous imaginal disc 1 (TID1) inhibits isoproterenol-induced cardiac hypertrophy and apoptosis by regulating c-terminus of hsc70-interacting protein (CHIP) mediated degradation of Gαs.

Chih-Chung Feng, Po-Hsiang Liao, Hsiang-I Tsai, Shiu-Min Cheng, Liang-Yo Yang, Vijaya PadmaViswanadha, Lung-Fa Pan, Ray-Jade Chen, Jeng-Fan Lo, Chih-Yang Huang

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 14 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

10 authors at 7 institutions in 2 countries.

Chih-Chung FengGraduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
Po-Hsiang LiaoGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Hsiang-I TsaiGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Shiu-Min ChengDepartment of Psychology, Asia University, Taichung, Taiwan.
Liang-Yo YangDepartment of Physiology, School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan.
Vijaya PadmaViswanadhaDepartment of Biotechnology, Bharathiar University, Coimbatore-641 046, India.
Lung-Fa PanCardiology Department of Taichung Armed Forced General Hospital, Taichung, Taiwan.
Ray-Jade ChenDepartment of Surgery, School of Medicine, Taipei Medical University, Taipei, Taiwan.
Jeng-Fan LoInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Chih-Yang HuangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
China Medical University · TWAsia University · TWBharathiar University · INCentral Taiwan University of Science and Technology · TWNational Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dilated cardiomyopathy (DCM) is the most common form of non-ischemic cardiomyopathy. It is characterized by ventricular chamber dilation, and myocyte hypertrophy. Human tumorous imaginal disc 1 (Tid1), a chaperone protein and response to regulate number of signaling molecules in the mitochondria or cytosol. Tid1 also plays a major role in preventing DCM; however, the role of Tid1 in isoproterenol (ISO)-induced cardiac apoptosis and hypertrophy remains unclear. H9c2 cells were pretreated Tid1 before ISO-induced hypertrophy and apoptosis and then evaluated by IHC, TUNEL assay, IFC, Co-IP, and Western blot. From the IHC experiment, we found that Tid1 proteins were increased in tissues from different stages of human myocardial infarction. Using H9c2 cardiomyoblast cells we found that Tid1 was decreased by ISO treatment. However, over-expression of Tid1S suppressed NFATc3, BNP and calcineurin protein expression and inhibited NFATc3 nuclear translocation in ISO induced cardiomyoblast cells. On the other hand, Tid1S over-expression activated survival proteins p-AKT

Indexed as

AnimalsApoptosisCardiomegalyHSP40 Heat-Shock ProteinsHumansIsoproterenolMaleRatsSignal TransductionTissue Array AnalysisUbiquitin-Protein LigasesHSP40 Heat-Shock ProteinsIsoproterenolStub1 protein, ratUbiquitin-Protein LigasesCHIPGαsH9c2hypertrophyisoproterenolTid1

Identifiers

PMID30443176
PMCPMC6216068
OpenAlexW2898308703

What OpenQuestion holds

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LicenceCC BY-NC
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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.