Evidence map›Paper›PMID 26515045›Full record

ArticleJournal of cellular and molecular medicine2016

Mas receptor mediates cardioprotection of angiotensin-(1-7) against Angiotensin II-induced cardiomyocyte autophagy and cardiac remodelling through inhibition of oxidative stress.

Li Lin, Xuebo Liu, Jianfeng Xu, Liqing Weng, Jun Ren, Junbo Ge, Yunzeng Zou

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.2field-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

37 citing papers in PubMed, 82 citations in OpenAlex.

  1. Imbalance of renin-angiotensin system in calcium oxalate crystals-induced renal oxidative stress and autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

7 authors at 4 institutions in 1 country.

Li LinDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Xuebo LiuDepartment 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.
Liqing WengDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Jun RenShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Junbo GeShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Yunzeng ZouShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Science, Fudan University, Shanghai, China.
Shanghai East Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (Ang II) plays an important role in the onset and development of cardiac remodelling associated with changes of autophagy. Angiotensin1-7 [Ang-(1-7)] is a newly established bioactive peptide of renin-angiotensin system, which has been shown to counteract the deleterious effects of Ang II. However, the precise impact of Ang-(1-7) on Ang II-induced cardiomyocyte autophagy remained essentially elusive. The aim of the present study was to examine if Ang-(1-7) inhibits Ang II-induced autophagy and the underlying mechanism involved. Cultured neonatal rat cardiomyocytes were exposed to Ang II for 48 hrs while mice were infused with Ang II for 4 weeks to induce models of cardiac hypertrophy in vitro and in vivo. LC3b-II and p62, markers of autophagy, expression were significantly elevated in cardiomyocytes, suggesting the presence of autophagy accompanying cardiac hypertrophy in response to Ang II treatment. Besides, Ang II induced oxidative stress, manifesting as an increase in malondialdehyde production and a decrease in superoxide dismutase activity. Ang-(1-7) significantly retarded hypertrophy, autophagy and oxidative stress in the heart. Furthermore, a role of Mas receptor in Ang-(1-7)-mediated action was assessed using A779 peptide, a selective Mas receptor antagonist. The beneficial responses of Ang-(1-7) on cardiac remodelling, autophagy and oxidative stress were mitigated by A779. Taken together, these result indicated that Mas receptor mediates cardioprotection of angiotensin-(1-7) against Ang II-induced cardiomyocyte autophagy and cardiac remodelling through inhibition of oxidative stress.

Indexed as

Angiotensin IIAnimalsAutophagyCardiomegalyCardiotonic AgentsCells, CulturedDrug Evaluation, PreclinicalMaleMice, Inbred C57BLMyocytes, CardiacOxidative StressPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsRats, Sprague-DawleyReceptors, G-Protein-Coupled7-Ala-angiotensin (1-7)Angiotensin IICardiotonic AgentsPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledangiotensin-(1-7)autophagyheart failureMasoxidative stress

Identifiers

PMID26515045
PMCPMC4717848
OpenAlexW1880710670

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.