Evidence map›Paper›PMID 14986170›Full record

ArticleJournal of human genetics2004

The role of a common TNNT2 polymorphism in cardiac hypertrophy.

Kazuo Komamura, Naoharu Iwai, Koichi Kokame, Yoshio Yasumura, Jiyoong Kim, Masakazu Yamagishi, Takayuki Morisaki, Akinori Kimura, Hitonobu Tomoike, Masafumi Kitakaze and 1 more

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In one paragraph

Article in Journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  12. RNA binding proteins in the regulation of heart development.The international journal of biochemistry & cell biology · 2013
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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

11 authors at 2 institutions in 1 country.

Kazuo KomamuraDepartment of Cardiovascular Dynamics, Research Institute, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita 565-8565, Japan. kkoma@hsp.ncvc.go.jp.
Naoharu IwaiDepartment of Epidemiology, Research Institute, National Cardiovascular Center, Suita, Japan.
Koichi KokameDepartment of Vascular Physiology, Research Institute, National Cardiovascular Center, Suita, Japan.
Yoshio YasumuraDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
Jiyoong KimDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
Masakazu YamagishiDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
Takayuki MorisakiDepartment of Bioscience, Research Institute, National Cardiovascular Center, Suita, Japan.
Akinori KimuraDepartment of Molecular Pathogenesis, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Hitonobu TomoikeDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
Masafumi KitakazeDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
Kunio MiyatakeDepartment of Cardiology, National Cardiovascular Center, Suita, Japan.
National Cerebral and Cardiovascular Center · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We found a five-basepair insertion/deletion polymorphism in intron 3 of TNNT2, one of the genes responsible for hypertrophic cardiomyopathy. These five bases may be part of an intronic polypyrimidine tract sequence that may affect splicing. The purpose of the study was to examine the association of the polymorphism with cardiac hypertrophy. The study population consisted of 151 subjects with prominent concentric left ventricular hypertrophy, and 987 healthy subjects recruited from medical checkups (control population). The deletion/deletion genotype tended to be associated with a larger left ventricular mass/height ratio in the HCM population ( p<0.0001). Multiple regression analyses indicated that the left ventricular mass/height ratio was determined ( p<0.0001, R=0.738) by the TNNT2 genotype. Moreover, the frequency of the deletion allele was significantly higher in the hypertrophy population than in the control population ( p<0.0001). In vitro expression study revealed the deletion allele significantly affected the mRNA expression pattern by skipping exon 4 during splicing. In conclusion, TNNT2 deletion allele could be associated with a predisposition to prominent left ventricular hypertrophy.

Indexed as

Polymorphism, GeneticAgedAllelesBase SequenceDNAFemaleGene DeletionGene FrequencyGenotypeHumansHypertrophy, Left VentricularIntronsMaleMiddle AgedMolecular Sequence DataPlasmidsDNATroponin T

Identifiers

PMID14986170
OpenAlexW2092825478

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.