Evidence map›Paper›PMID 30341569›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2018

AdipoRon, an adiponectin receptor agonist, attenuates cardiac remodeling induced by pressure overload.

Ning Zhang, Wen-Ying Wei, Hai-Han Liao, Zheng Yang, Can Hu, Sha-Sha Wang, Wei Deng, Qi-Zhu Tang

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 45 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

8 authors at 3 institutions in 1 country.

Ning ZhangDepartment of Cardiology, Affiliated Hospital of Qingdao University, Qingdao, China.
Wen-Ying WeiDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Hai-Han LiaoDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Zheng YangDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Can HuDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Sha-Sha WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China. vivideng1982@whu.edu.cn.
Qi-Zhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China. qztang@whu.edu.cn.
Renmin Hospital of Wuhan University · CNAffiliated Hospital of Qingdao University · CNWuhan University · CN

Funding

National Major Scientific Instrument and Equipment Development Projects 2013YQ03092306National Natural Science Foundation of China 81470516, 81270303the Key Project of the National Natural Science Foundation 81530012The prevention and control project of cardiovascular disease 2016ZX-008-01
6 · The paper itself

Abstract

AdipoRon, a small-molecule adiponectin receptor (AdipoR) agonist, has been reported to be implicated in cardiovascular diseases. However, its role in pressure-overload-induced cardiac remodeling is still elusive. To elucidate the role of AdipoRon in the pathogenesis of cardiac remodeling in vivo and vitro, in the left ventricle of human end-stage heart failure, the expression of AdipoR2 is upregulated. Meanwhile, increased expression of AdipoR2 was also observed in mice failing hearts. Oral administration of AdipoRon alleviated cardiac hypertrophy and fibrosis induced by pressure overload, as evidenced by the beneficial change of cross-sectional area of cardiomyocytes, heart weight-to-body weight ratio, gene expression of hypertrophic markers, ventricle collagen ratio, and cardiac function. The AMPKα activation mediated by AdipoRon significantly inhibited AngII-induced TGF-β1 expression and cardiac fibroblast differentiation, and these inhibitory effects were abrogated by treatment with the AMPK inhibitor Compound C. Consistent with the above results, AdipoRon abolished the ability to retard AngII-induced TGF-β1 expression in AMPKα2

Indexed as

AMP-Activated Protein KinasesAngiotensin IIAnimalsBlood PressureCardiomegalyCell DifferentiationFibroblastsHumansMaleMice, Inbred C57BLMice, KnockoutPiperidinesRats, Sprague-DawleyReceptors, AdiponectinTransforming Growth Factor beta1Ventricular RemodelingAdipoRonAMP-Activated Protein KinasesAngiotensin IIPiperidinesPrkaa2 protein, mouseReceptors, AdiponectinTransforming Growth Factor beta1AdipoRonAMP-activated protein kinaseCardiac remodelingMyofibroblast differentiationTGF-β1

Identifiers

PMID30341569
OpenAlexW2895872914

What OpenQuestion holds

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Registered trials

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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.