Evidence map›Paper›PMID 28849157›Full record

ArticleMolecular medicine reports2017

Molecular characterization of a pedigree carrying the hypertension‑associated mitochondrial tRNAGln T4363C mutation.

Lei Wang, Zhibing Dong, Wenhui Lin, Ranran Gao, Caiming Chen, Jinzhong Xu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Novel mitochondrial tRNAIrish journal of medical science · 2023
    Article
  2. Potential Roles of mtDNA Mutations in PCOS-IR: A Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Review
  3. Article
  4. The Role of Mitochondrial DNA Mutations in Cardiovascular Diseases.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Mitochondrial tRNAIrish journal of medical science · 2020
    Article
  7. 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

6 authors at 1 institution in 1 country.

Lei WangDepartment of Cardiology, Hanchuan People's Hospital, Hanchuan, Hubei 431600, P.R. China.
Zhibing DongDepartment of Cardiology, The Affiliated Wenling Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 317500, P.R. China.
Wenhui LinDepartment of Cardiology, The Affiliated Wenling Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 317500, P.R. China.
Ranran GaoDepartment of Cardiology, The Affiliated Wenling Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 317500, P.R. China.
Caiming ChenDepartment of Clinical Pharmacy, The Affiliated Wenling Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 317500, P.R. China.
Jinzhong XuDepartment of Clinical Pharmacy, The Affiliated Wenling Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 317500, P.R. China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial DNA mutations have been reported to be associated with essential hypertension. The present study reported the clinical and molecular features of a Chinese pedigree with maternally inherited hypertension. A total of 6 matrilineal relatives in this pedigree presented with variable degrees of hypertension; the age of onset ranged between 39 and 63 years, and the average age of onset was 53 years. Analysis of the mitochondrial genome in members of this family demonstrated the occurrence of a homoplasmic T4363C mutation in the transfer (t)RNAGln gene and 25 genetic polymorphisms belonging to mitochondrial haplogroup B4. Notably, the T4363C mutation was localized at the anticodon stem of tRNAGln, which is highly conserved across various species (conventional position 38). To determine its potential pathogenicity, RNA Fold software was used to predict the secondary structure of tRNAGln with and without this mutation. The results indicated that the T4363C mutation induced a significant alteration in the secondary structure of tRNAGln, and may reduce the steady‑state levels of tRNAGln. Furthermore, matrilineal relatives carrying the T4363C mutation exhibited different age of onset and variable degrees of blood pressure, thus indicating that the T4363C mutation itself was insufficient to produce the clinical phenotype. Therefore, other modified factors, including environmental factors, and nuclear gene and epigenetic modifications, may be involved in the pathogenesis of hypertension. In conclusion, the present study provided valuable information regarding the association between tRNA mutations and hypertension.

Indexed as

Genetic Predisposition to DiseasePoint MutationAdultAgedAsian PeopleBase SequenceFemaleHumansHypertensionMaleMaternal InheritanceMiddle AgedNucleic Acid ConformationPedigreePhenotypeRNARNARNA, MitochondrialRNA, Transfer, Gln

Identifiers

PMID28849157
PMCPMC5865805
OpenAlexW2749704847

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.