Evidence map›Paper›PMID 28181410›Full record

ArticleJournal of cellular and molecular medicine2017

Sestrin 1 ameliorates cardiac hypertrophy via autophagy activation.

Ruicong Xue, Junyi Zeng, Yili Chen, Cong Chen, Weiping Tan, Jingjing Zhao, Bin Dong, Yu Sun, Yugang Dong, Chen Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.0field-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

31 citing papers in PubMed, 51 citations in OpenAlex.

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  15. Observational
  16. Article
  17. Sestrins in Physiological Stress Responses.Annual review of physiology · 2021
    Review
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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 2 institutions in 1 country.

Ruicong XueDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Junyi ZengDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Yili ChenDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Cong ChenDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Weiping TanDepartment of Respiratory, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Jingjing ZhaoDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Bin DongDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Yu SunDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Yugang DongDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Chen LiuDepartment of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is one of the major risk factors of cardiovascular morbidity and mortality. Autophagy is acknowledged to be an important mechanism regulating cardiac hypertrophy. Sestrin 1, a downstream target gene of p53, has been proven to regulate autophagy. However, the role of Sestrin 1 in cardiac hypertrophy remains unknown. Our study showed that Sestrin 1 mRNA and protein expression declined in pressure overload cardiac hypertrophy and phenylephrine (PE)-induced cardiac hypertrophy. Knockdown of Sestrin 1 by RNAi deteriorated PE-induced cardiac hypertrophy, whereas the overexpression of Sestrin 1 by adenovirus transfection blunted hypertrophy. We discovered that knockdown of Sestrin 1 resulted in impaired autophagy while overexpression of Sestrin 1 resulted in increased autophagy without affecting lysosomal function. In addition, the antihypertrophic effect of Sestrin 1 overexpression was eliminated by autophagy blockade. Importantly, Sestrin 1 targets at the AMPK/mTORC1/autophagy pathway to inhibit cardiac hypertrophy by interaction with AMPK which is responsible for autophagy regulation. Taken together, our data indicate that Sestrin 1 regulates AMPK/mTORC1/autophagy axis to attenuate cardiac hypertrophy.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsAutophagyCardiomegalyCell Cycle ProteinsGene Expression RegulationGene Knockdown TechniquesHumansMechanistic Target of Rapamycin Complex 1MicePhenylephrinePhosphorylationProtein KinasesRatsSestrinsSignal TransductionAMP-Activated Protein Kinase KinasesCell Cycle ProteinsMechanistic Target of Rapamycin Complex 1PhenylephrineProtein KinasesSesn1 protein, mouseSestrinsAMPKautophagycardiac hypertrophyphenylephrineSestrin 1

Identifiers

PMID28181410
PMCPMC5431155
OpenAlexW2587046652

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.