Evidence map›Paper›PMID 32964914›Full record

ArticleBioscience reports2020

Sophoricoside ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy.

Maomao Gao, Fengjiao Hu, Manli Hu, Yufeng Hu, Hongjie Shi, Guo-Jun Zhao, Chongshu Jian, Yan-Xiao Ji, Xiao-Jing Zhang, Zhi-Gang She and 2 more

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 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

12 authors at 1 institution in 1 country.

Maomao Gao *Medical Research Institute, Wuhan University, Wuhan 430072, China.
Fengjiao Hu *Medical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Manli HuMedical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Yufeng HuMedical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Hongjie ShiInstitute of Model Animal of Wuhan University, Luojia Mount Wuchang, Wuhan 430072, China.
Guo-Jun ZhaoDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Chongshu JianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Yan-Xiao JiMedical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Xiao-Jing ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Zhi-Gang SheDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Hongliang Li *Medical Research Institute, Wuhan University, Wuhan 430072, China.
Lihua Zhu *Institute of Model Animal of Wuhan University, Luojia Mount Wuchang, Wuhan 430072, China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe study aims to evaluate protective effects of sophoricoside (Sop) on cardiac hypertrophy. Meanwhile, the potential and significance of Sop should be broadened and it should be considered as an attractive drug for the treatment of pathological cardiac hypertrophy and heart failure.

methodsUsing the phenylephrine (PE)-induced neonatal rat cardiomyocytes (NRCMs) enlargement model, the potent protection of Sop against cardiomyocytes enlargement was evaluated. The function of Sop was validated in mice received transverse aortic coarctation (TAC) or sham surgery. At 1 week after TAC surgery, mice were treated with Sop for the following 4 weeks, the hearts were harvested after echocardiography examination.

resultsOur study revealed that Sop significantly mitigated TAC-induced heart dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis. Mechanistically, Sop treatment induced a remarkable activation of AMPK/mTORC1-autophagy cascade following sustained hypertrophic stimulation. Importantly, the protective effect of Sop was largely abolished by the AMPKα inhibitor Compound C, suggesting an AMPK activation-dependent manner of Sop function on suppressing pathological cardiac hypertrophy.

conclusionSop ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy. Hence, Sop might be an attractive candidate for the treatment of pathological cardiac hypertrophy and heart failure.

Indexed as

AMP-Activated Protein KinasesAnimalsAutophagyBenzopyransCardiomegalyCells, CulturedCell SizeDisease Models, AnimalEnzyme ActivationEnzyme ActivatorsFibrosisMaleMechanistic Target of Rapamycin Complex 1MiceMyocytes, CardiacRats, Sprague-DawleyAMP-Activated Protein KinasesBenzopyransEnzyme ActivatorsMechanistic Target of Rapamycin Complex 1sophoricosideAMPKautophagycardiac hypertrophySophoricoside

Identifiers

PMID32964914
PMCPMC7677750
OpenAlexW3087932446

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.