Evidence map›Paper›PMID 31424159›Full record

ArticleJournal of cellular and molecular medicine2019

Novel polymorphisms in PDLIM3 and PDLIM5 gene encoding Z-line proteins increase risk of idiopathic dilated cardiomyopathy.

Dongfei Wang, Juan Fang, Jialan Lv, Zhicheng Pan, Xiang Yin, Hongqiang Cheng, Xiaogang Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022
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  17. The unexpected versatility of ALP/Enigma family proteins.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
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  20. Frontiers in genetics · 2021
    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 2 institutions in 1 country.

Dongfei WangDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Juan FangDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jialan LvDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhicheng PanDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiang YinDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Hongqiang ChengDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou, China.
Xiaogang GuoDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6754-1432
First Affiliated Hospital Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic dilated cardiomyopathy (IDCM), characterized by ventricular dilation and impaired systolic function, is a primary cardiomyopathy resulting in heart failure. During heart contraction, the Z-line is responsible for transmitting force between sarcomeres and is also a hot spot for muscle cell signalling. Mutations in Z-line proteins have been linked to cardiomyopathies in both humans and mice. Actinin-associated LIM protein (ALP) and enigma homolog protein (ENH), encoded by PDLIM3 and PDLIM5, are components of the muscle cytoskeleton and localize to the Z-line. A PDLIM3 or PDLIM5 deficiency in mice leads to dilated cardiomyopathy. Since PDLIM3 and PDLIM5 are candidate IDCM susceptibility genes, the current study aims to investigate whether polymorphisms within PDLIM3 and PDLIM5 could be correlated with IDCM. We designed a case-control study, and exons of the PDLIM3 and PDLIM5 were amplified by polymerase chain reactions in 111 IDCM patients and 137 healthy controls. We found that five synonymous polymorphisms had statistical distribution differences between IDCM patients and controls, including rs4861669, rs4862543, c.731 + 131 T > G, c.1789-3 C > T and rs7690296, according to genotype and allele distribution. Haplotype G-C-C-C and A-T-C-T (rs2306705, rs10866276, rs12644280 and rs4635850 synthesized) were regarded as risk factors for IDCM patients when compared with carriers of other haplotypes (all P < .05). Furthermore, IDCM patients with two novel polymorphisms (c.731 + 131 T > G and c.1789-3 C > T) had lower systolic blood pressure. In conclusion, these five synonymous polymorphisms might constitute a genetic background that increases the risk of the development of IDCM in the Chinese Han population.

Indexed as

Genetic Predisposition to DiseaseAdaptor Proteins, Signal TransducingAllelesBlood PressureCardiomyopathy, DilatedCase-Control StudiesEthnicityFemaleHaplotypesHumansLIM Domain ProteinsLinkage DisequilibriumMaleMicrofilament ProteinsMiddle AgedPolymorphism, Single NucleotideAdaptor Proteins, Signal TransducingLIM Domain ProteinsMicrofilament ProteinsPDLIM3 protein, humanPDLIM5 protein, humanidiopathic dilated cardiomyopathyPDLIM3PDLIM5polymorphism

Identifiers

PMID31424159
PMCPMC6787498
OpenAlexW2969533241

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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.