Evidence map›Paper›PMID 25820336›Full record

ArticleCirculation2015

Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9.

Xuan Wei, Bing Wu, Jing Zhao, Zhi Zeng, Wanling Xuan, Shiping Cao, Xiaobo Huang, Masanori Asakura, Dingli Xu, Jianping Bin and 2 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 78 citations in OpenAlex.

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  17. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Xuan WeiFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Bing WuFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Jing ZhaoFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Zhi ZengFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Wanling XuanFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Shiping CaoFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Xiaobo HuangFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Masanori AsakuraFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Dingli XuFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Jianping BinFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Masafumi KitakazeFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.).
Yulin LiaoFrom Sate Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, China (X.W., B.W., J.Z., Z.Z., W.X., S.C., X.H., D.X., J.B., M.K., Y.L.); and Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (M.A., M.K.). liao18@msn.com kitakaze@zf6.so-net.ne.jp.
National Cerebral and Cardiovascular Center · JPSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransient preceding brief ischemia provides potent cardioprotection against subsequent long ischemia, termed ischemic preconditioning. Here, we hypothesized that transient short-term hypertrophic stimulation would induce the expression of hypertrophy regression genes and render the heart resistant to subsequent hypertrophic stress, and slow the progression to heart failure, as well. METHODS AND

resultsCardiomyocyte hypertrophy was induced in mice by either transverse aortic constriction or an infusion of phenylephrine, and in neonatal rat ventricular cardiomyocytes by norepinephrine exposures. In the preconditioning groups, hypertrophic stimulation was provided for 1 to 7 days and then withdrawn for several days by either aortic debanding or discontinuing phenylephrine or norepinephrine treatment, followed by subsequent reexposure to the hypertrophic stimulus for the same period as in the control group. One or 6 weeks after transverse aortic constriction, the heart weight/body weight ratio was lower in the preconditioning group than in the control group, whereas the lung weight/body weight ratio was significantly decreased 6 weeks after transverse aortic constriction. Similar results were obtained in mice receiving phenylephrine infusion and neonatal rat ventricular cardiomyocytes stimulated with norepinephrine. Both mRNA and protein expression of S100A8 and S100A9 showed significant upregulation after the removal of hypertrophic stimulation and persisted for 6 weeks in response to reimposition of transverse aortic constriction. The treatment with recombinant S100A8/A9 inhibited norepinephrine-induced myocyte hypertrophy and reduced the expression of calcineurin and NFATc3, but the silencing of S100A8/A9 prevented such changes.

conclusionsPreconditioning with prohypertrophic factors exerts an antihypertrophic effect and slows the progression of heart failure, indicating the existence of the phenomenon for hypertrophic preconditioning.

Indexed as

AnimalsAortic Valve StenosisCalcineurinCalgranulin ACalgranulin BCardiomyopathy, HypertrophicCells, CulturedDisease Models, AnimalDisease ProgressionGene Expression RegulationGenetic VectorsHeart FailureHypertrophyMaleMiceMice, Inbred C57BLCalcineurinCalgranulin ACalgranulin BNFATC Transcription FactorsPhenylephrineRecombinant Fusion ProteinsRNA, MessengerS100A9 protein, mousetranscription factor NF-AT c3cardiomegalyheart failuremyocardial preconditioningS100A8 proteinS100A9 protein

Identifiers

PMID25820336
PMCPMC4415966
OpenAlexW1987343336

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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.