Evidence map›Paper›PMID 25116394›Full record

ArticlePloS one2014

Hypoxia preconditioned mesenchymal stem cells prevent cardiac fibroblast activation and collagen production via leptin.

Panpan Chen, Rongrong Wu, Wei Zhu, Zhi Jiang, Yinchuan Xu, Han Chen, Zhaocai Zhang, Huiqiang Chen, Ling Zhang, Hong Yu and 2 more

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
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. It has been retracted, and should not be counted. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Panpan ChenDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Rongrong WuDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Wei ZhuDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Zhi JiangDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Yinchuan XuDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Han ChenDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Zhaocai ZhangDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Huiqiang ChenDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Ling ZhangDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Hong YuDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Jian'an WangDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Xinyang HuDivision of Cardiology, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Zhejiang Province, Hangzhou, China; Provincial Key Laboratory of Cardiovascular Research, Zhejiang Province, Hangzhou, China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

Analysis: Emotion-Based Alcohol Consumption with fMRI and Experimental ParadigmK01AA020102 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI CYDERS, MELISSA A · 2011 to 2015
$770k
NIAAA NIH HHS K01 AA020102
6 · The paper itself

Abstract

aimsActivation of cardiac fibroblasts into myofibroblasts constitutes a key step in cardiac remodeling after myocardial infarction (MI), due to interstitial fibrosis. Mesenchymal stem cells (MSCs) have been shown to improve post-MI remodeling an effect that is enhanced by hypoxia preconditioning (HPC). Leptin has been shown to promote cardiac fibrosis. The expression of leptin is significantly increased in MSCs after HPC but it is unknown whether leptin contributes to MSC therapy or the fibrosis process. The objective of this study was to determine whether leptin secreted from MSCs modulates cardiac fibrosis.

methodsCardiac fibroblast (CF) activation was induced by hypoxia (0.5% O2). The effects of MSCs on fibroblast activation were analyzed by co-culturing MSCs with CFs, and detecting the expression of α-SMA, SM22α, and collagen IαI in CFs by western blot, immunofluorescence and Sirius red staining. In vivo MSCs antifibrotic effects on left ventricular remodeling were investigated using an acute MI model involving permanent ligation of the left anterior descending coronary artery.

resultsCo-cultured MSCs decreased fibroblast activation and HPC enhanced the effects. Leptin deficit MSCs from Ob/Ob mice did not decrease fibroblast activation. Consistent with this, H-MSCs significantly inhibited cardiac fibrosis after MI and mediated decreased expression of TGF-β/Smad2 and MRTF-A in CFs. These effects were again absent in leptin-deficient MSCs.

conclusionOur data demonstrate that activation of cardiac fibroblast was inhibited by MSCs in a manner that was leptin-dependent. The mechanism may involve blocking TGF-β/Smad2 and MRTF-A signal pathways.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsCell DifferentiationCollagenGene ExpressionHypoxiaLeptinMesenchymal Stem CellsMiceMyocardial InfarctionMyofibroblastsSignal TransductionSmad2 ProteinTrans-ActivatorsTransforming Growth Factor betaVentricular RemodelingCollagenLeptinMrtfa protein, mouseSmad2 ProteinTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID25116394
PMCPMC4130526
OpenAlexW2014287951

What OpenQuestion holds

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LicenceCC BY
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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.