Evidence map›Paper›PMID 29626209›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2018

XRCC3 polymorphism is associated with hypertension-induced left ventricular hypertrophy.

Andi Ariyandy, Chiemi Sakai, Mari Ishida, Ryusei Mizuta, Kiyoshi Miyagawa, Satoshi Tashiro, Aiko Kinomura, Koji Hiraaki, Keitaro Ueda, Masao Yoshizumi and 1 more

Abstract read
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In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
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 4 institutions in 1 country.

Andi AriyandyDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Chiemi SakaiDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Mari IshidaDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan. mari@hiroshima-u.ac.jp.
Ryusei MizutaDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Kiyoshi MiyagawaLaboratory of Molecular Radiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Satoshi TashiroResearch Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Aiko KinomuraResearch Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Koji HiraakiMinamikaita Hospital, Hiroshima, Japan.
Keitaro UedaDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Masao YoshizumiDepartment of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Takafumi IshidaDepartment of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan.
Hiroshima University · JPFukushima Medical University · JPHiroshima Minami High School · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficiency of X-ray repair cross-complementing protein 3 (XRCC3), a DNA-damage repair molecule, and the 241Met variant of XRCC3 have been reported to increase endoreduplication, which induces polyploidy. The aims of this study were to determine the impact of the XRCC3 polymorphism on the incidence of hypertension-induced left ventricular hypertrophy (LVH) and to investigate the mechanisms underlying any potential relationship. Patients undergoing chronic hemodialysis (n = 77) were genotyped to assess for the XRCC3 Thr241Met polymorphism. The XRCC3 241Thr/Met genotype was more frequent in the LVH (+) group than in the LVH (-) group (42.3 vs. 13.7%, χ2 = 7.85, p = 0.0051). To investigate possible mechanisms underlying these observations, human XRCC3 cDNA of 241Thr or that of 241Met was introduced into cultured CHO cells. The surface area of CHO cells expressing XRCC3 241Met was larger than that expressing 241Thr. Spontaneous DNA double-strand breaks accumulated to a greater degree in NIH3T3 cells expressing 241Met (3T3-241Met) than in those expressing 241Thr (3T3-241Thr). DNA damage caused by radiation induced cell senescence more frequently in 3T3-241Met. The levels of basal and TNF-α-stimulated MCP-1 mRNA and protein secretion were higher in 3T3-241Met. Finally, FACS analysis revealed that the cell percentage in G2/M phase including polyploidy was significantly higher in 3T3-241Met than in 3T3-241Thr. Furthermore, the basal level of MCP-1 mRNA positively correlated with the cell percentage in G2/M phase and polyploidy. These data suggest that the XRCC3 241Met increases the risk of LVH via accumulation of DNA damage, thereby altering cell cycle progression and inducing cell senescence and a proinflammatory phenotype.

Indexed as

AgedAged, 80 and overAnimalsCHO CellsCricetulusDNA-Binding ProteinsFemaleHumansHypertensionHypertrophy, Left VentricularMaleMiceMiddle AgedNIH 3T3 CellsDNA-Binding ProteinsX-ray repair cross complementing protein 3

Identifiers

PMID29626209
OpenAlexW2797509664

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.