Evidence map›Paper›PMID 25946687›Full record

ArticleJournal of cellular and molecular medicine2015

High-density lipoprotein inhibits mechanical stress-induced cardiomyocyte autophagy and cardiac hypertrophy through angiotensin II type 1 receptor-mediated PI3K/Akt pathway.

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, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  8. Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2023
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  14. HDL Composition, Heart Failure, and Its Comorbidities.Frontiers in cardiovascular medicine · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. HDL subclasses and mortality in acute heart failure patients.Clinica chimica acta; international journal of clinical chemistry · 2019
    Article
  20. Article
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.
Tongji University · 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

Mechanical stress triggers cardiac hypertrophy and autophagy through an angiotensin II (Ang II) type 1 (AT1) receptor-dependent mechanism. Low level of high density lipoprotein (HDL) is an independent risk factor for cardiac hypertrophy. This study was designed to evaluate the effect of HDL on mechanical stress-induced cardiac hypertrophy and autophagy. A 48-hr mechanical stretch and a 4-week transverse aortic constriction were employed to induce cardiomyocyte hypertrophy in vitro and in vivo, respectively, prior to the assessment of myocardial autophagy using LC3b-II and beclin-1. Our results indicated that HDL significantly reduced mechanical stretch-induced rise in autophagy as demonstrated by LC3b-II and beclin-1. In addition, mechanical stress up-regulated AT1 receptor expression in both cultured cardiomyocytes and in mouse hearts, whereas HDL significantly suppressed the AT1 receptor. Furthermore, the role of Akt phosphorylation in HDL-mediated action was assessed using MK-2206, a selective inhibitor for Akt phosphorylation. Our data further revealed that MK-2206 mitigated HDL-induced beneficial responses on cardiac remodelling and autophagy. Taken together, our data revealed that HDL inhibited mechanical stress-induced cardiac hypertrophy and autophagy through downregulation of AT1 receptor, and HDL ameliorated cardiac hypertrophy and autophagy via Akt-dependent mechanism.

Indexed as

Stress, MechanicalAnimalsAutophagyCardiomegalyCardiotonic AgentsCells, CulturedDown-RegulationLipoproteins, HDLMaleMice, Inbred C57BLMyocytes, CardiacPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRats, Sprague-DawleyReceptor, Angiotensin, Type 1Cardiotonic AgentsLipoproteins, HDLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Angiotensin, Type 1AT1 receptorautophagycardiac hypertrophyHDLheart failure

Identifiers

PMID25946687
PMCPMC4549043
OpenAlexW1578111463

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.