Evidence map›Paper›PMID 31373621›Full record

ArticleCardiovascular research2020

HuR regulates phospholamban expression in isoproterenol-induced cardiac remodelling.

Han Hu, Mingyang Jiang, Yangpo Cao, Zhuojun Zhang, Bin Jiang, Feng Tian, Juan Feng, Yali Dou, Myriam Gorospe, Ming Zheng and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  14. Article
  15. Genetic landscape of phospholamban cardiomyopathies.Frontiers in cell and developmental biology · 2025
    Review
  16. Article
  17. Article
  18. RNA binding proteins as mediators of pathological cardiac remodeling.Frontiers in cell and developmental biology · 2024
    Review
  19. 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

13 authors at 4 institutions in 2 countries.

Han Hu>Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Mingyang JiangDepartment of Cardiology, State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210061, China.
Yangpo CaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road Beijing, 100191, China.
Zhuojun Zhang>Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Bin Jiang>Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Feng TianDepartment of Laboratory Animal Science, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Juan FengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road Beijing, 100191, China.
Yali DouDepartment of Pathology and Biological Chemistry, University of Michigan, 1301 Catherine Street, Ann Arbor, MI 48105, USA.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, 251 Bayview Blvd, Baltimore, MD 21224, USA.
Ming ZhengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road Beijing, 100191, China.
Lemin ZhengInstitute of Cardiovascular Research, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Zhongzhou YangDepartment of Cardiology, State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210061, China.
Wengong Wang>Department of Biochemistry and Molecular Biology, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100191, China.
Peking University · CNModel Animal Research Center · CNNational Institutes of Health · USUniversity of Michigan · US

Funding

Post-transcriptional Regulation Of Proliferative and Stress Response GenesZIAAG000511 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$25.4M
Post-transcriptional regulation of energy usage: glucose and lipid metabolismZIAAG000394 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$18.7M
6 · The paper itself

Abstract

aimsThe elevated expression of phospholamban (PLB) has been observed in heart failure and cardiac remodelling, inhibiting the affinity of Ca2+ pump to Ca2+ thereby impairing heart relaxation. However, the mechanisms underlying the regulation of PLB remains to be further studied. The present study aims to test the role of RNA-binding protein HuR in the regulation of PLB and the impact of this regulatory process in cardiac remodelling. METHODS AND

resultsA mouse model specifically deleted HuR in cardiomyocytes were used for testing the role of HuR in regulating PLB during isoproterenol (ISO)-induced cardiac remodelling. HuR deficiency did not significantly influence the phenotype and function of mouse heart under static status. However, deletion of HuR in cardiomyocytes mitigated the effect of ISO in inducing PLB expression and reducing β1-AR expression, in turn aggravating ISO-induced myocardial hypertrophy and cardiac fibrosis. In H9C2 cells, association of HuR with PLB and β1-AR mRNAs stabilized PLB mRNA and destabilized β1-AR mRNA, respectively.

conclusionHuR stabilizes PLB mRNA and destabilizes β1-AR mRNA. The HuR-PLB and HuR-β1-AR regulatory processes impact on ISO-induced cardiac remodelling.

Indexed as

IsoproterenolVentricular Function, LeftVentricular RemodelingAnimalsCalcium-Binding ProteinsCalcium SignalingCell LineDisease Models, AnimalELAV-Like Protein 1FibrosisHypertrophy, Left VentricularMice, Inbred C57BLMice, KnockoutMyocytes, CardiacPhospholambanPhosphorylationAdrb1 protein, mouseAdrb1 protein, ratCalcium-Binding ProteinsElavl1 protein, mouseElavl1 protein, ratELAV-Like Protein 1IsoproterenolPhospholambanReceptors, Adrenergic, beta-1RNA, MessengerCardiac remodellingHuRmRNA turnoverPLBβ1-AR

Identifiers

PMID31373621
PMCPMC7868665
OpenAlexW2966419536

What OpenQuestion holds

Textmetadata
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.