Evidence map›Paper›PMID 24465706›Full record

ArticlePloS one2014

Mechanisms of Ghrelin anti-heart failure: inhibition of Ang II-induced cardiomyocyte apoptosis by down-regulating AT1R expression.

Chunyan Yang, Zhonghui Liu, Kai Liu, Ping Yang

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 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.4field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. New and future heart failure drugs.Nature cardiovascular research · 2024
    Review
  4. Article
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  11. Ghrelin Alleviates Angiotensin II-Induced H9c2 Apoptosis: Impact of the miR-208 Family.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
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  20. MicroRNA-1 in Cardiac Diseases and Cancers.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014
    Review
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

4 authors at 3 institutions in 1 country.

Chunyan YangDepartment of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
Zhonghui LiuDepartment of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China ; Department of Immunology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Kai LiuDepartment of Hepatobiliary and Pancreatic Surgery, First Hospital, Jilin University, Changchun, China.
Ping YangDepartment of Cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
Union Hospital · CNFirst Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGhrelin is a novel growth hormone-releasing peptide administered to treat chronic heart failure (CHF). However, the underlying mechanism of its protective effects against heart failure (HF) remains unclear. METHODS AND

resultsA total of 68 patients with CHF and 20 healthy individuals were included. The serum levels of Angiotensin II (Ang II) and ghrelin were measured using ELISA. The results showed that Ang II and ghrelin were both significantly increased in CHF patients and that the ghrelin levels were significantly positively correlated with Ang II. The left anterior descending coronary artery was ligated to establish a rat model of CHF, and cultured cardiomyocytes from neonatal rats were stimulated with Ang II to explore the role of ghrelin in CHF. The results showed that ghrelin inhibited cardiomyocyte apoptosis both in vivo and in vitro. Furthermore, caspase-3 expression was examined, and the results revealed that Ang II induces cardiomyocyte apoptosis through the caspase-3 pathway, whereas ghrelin inhibits this action. Lastly, to further elucidate the mechanism by which ghrelin inhibits Ang II action, the expression of the AT1 and AT2 receptors was evaluated; the results showed that Ang II up-regulates the AT1 and AT2 receptors in cardiomyocytes, whereas ghrelin inhibits AT1 receptor up-regulation but does not affect AT2 receptor expression.

conclusionsThese data suggest that the serum levels of ghrelin are significantly positively correlated with Ang II in CHF patients and that ghrelin can inhibit Ang II-induced cardiomyocyte apoptosis by down-regulating AT1R, thereby playing a role in preventing HF.

Indexed as

Angiotensin IIAnimalsApoptosisCase-Control StudiesCaspase 3Down-RegulationFemaleGhrelinHeart FailureHumansMaleMiddle AgedMyocardiumMyocytes, CardiacRatsRats, WistarAngiotensin IICaspase 3GhrelinReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2RNA, Messenger

Identifiers

PMID24465706
PMCPMC3897516
OpenAlexW2169729063

What OpenQuestion holds

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LicenceCC BY
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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.