Evidence map›Paper›PMID 24586922›Full record

ArticlePloS one2014

Mechanical stress triggers cardiomyocyte autophagy through angiotensin II type 1 receptor-mediated p38MAP kinase independently of angiotensin II.

Li Lin, Chuyi Tang, Jianfeng Xu, Yong Ye, Liqing Weng, Wei Wei, Junbo Ge, Xuebo Liu, Yunzeng Zou

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

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  14. The role of autophagy in cardiac hypertrophy.Acta biochimica et biophysica Sinica · 2016
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  17. Regulation of macroautophagy in amiodarone-induced pulmonary fibrosis.The journal of pathology. Clinical research · 2015
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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 6 institutions in 1 country.

Li LinDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Chuyi TangDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Jianfeng XuShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Yong YeShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Liqing WengShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Wei WeiDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Junbo GeShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Xuebo LiuDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Yunzeng ZouShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Shanghai East Hospital · CNTongji University · CNZhongshan Hospital · CNFudan University · CNSun 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

Angiotensin II (Ang II) type 1 (AT1) receptor is known to mediate a variety of physiological actions of Ang II including autophagy. However, the role of AT1 receptor in cardiomyocyte autophagy triggered by mechanical stress still remains elusive. The aim of this study was therefore to examine whether and how AT1 receptor participates in cardiomyocyte autophagy induced by mechanical stresses. A 48-hour mechanical stretch and a 4-week transverse aorta constriction (TAC) were imposed to cultured cardiomyocytes of neonatal rats and adult male C57B/L6 mice, respectively, to induce cardiomyocyte hypertrophy prior to the assessment of cardiomyocyte autophagy using LC3b-II. Losartan, an AT1 receptor blocker, but not PD123319, the AT2 inhibitor, was found to significantly reduce mechanical stretch-induced LC3b-II upregulation. Moreover, inhibition of p38MAP kinase attenuated not only mechanical stretch-induced cardiomyocyte hypertrophy but also autophagy. To the contrary, inhibition of ERK and JNK suppressed cardiac hypertrophy but not autophagy. Intriguingly, mechanical stretch-induced autophagy was significantly inhibited by Losartan in the absence of Ang II. Taken together, our results indicate that mechanical stress triggers cardiomyocyte autophagy through AT1 receptor-mediated activation of p38MAP kinase independently of Ang II.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingAngiotensin IIAnimalsBiomechanical PhenomenaCardiomegalyCells, CulturedChlorocebus aethiopsCOS CellsMaleMiceMice, Inbred C57BLMyocytes, Cardiacp38 Mitogen-Activated Protein KinasesRatsStress, PhysiologicalAdaptor Proteins, Signal TransducingAgtrap protein, mouseAngiotensin IIp38 Mitogen-Activated Protein Kinases

Identifiers

PMID24586922
PMCPMC3931796
OpenAlexW2025362788

What OpenQuestion holds

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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.