ArticleMolecular medicine reports2017
Molecular characterization of a pedigree carrying the hypertension‑associated mitochondrial tRNAGln T4363C mutation.
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.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Novel mitochondrial tRNAIrish journal of medical science · 2023Article
- Potential Roles of mtDNA Mutations in PCOS-IR: A Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Review
- Mutational analysis of mitochondrial tRNA genes in 138 patients with Leber's hereditary optic neuropathy.Irish journal of medical science · 2022Article
- The Role of Mitochondrial DNA Mutations in Cardiovascular Diseases.International journal of molecular sciences · 2022Review
- Associations of mitochondrial DNA 3777-4679 region mutations with maternally inherited essential hypertensive subjects in China.BMC medical genetics · 2020Article
- Mitochondrial tRNAIrish journal of medical science · 2020Article
- Comment on "Role of Mitochondrial Genome Mutations in Pathogenesis of Carotid Atherosclerosis".Oxidative medicine and cellular longevity · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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