Journal
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Volume 8, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2020.634137
Keywords
tRNA; mtDNA; hypertension; maternal; mutation
Categories
Funding
- Chinese National Natural Science Foundation of YL [81470542, 82070434]
- Chinese PLA General Hospital Young Medical Project [QNC19041]
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Essential hypertension is a common cardiovascular disease influenced by genetic and environmental factors, including mitochondrial DNA mutations. These mutations alter tRNA structure and lead to metabolic disorders, affecting protein synthesis and oxidative phosphorylation.
Essential hypertension (EH) is one of the most common cardiovascular diseases worldwide, entailing a high level of morbidity. EH is a multifactorial disease influenced by both genetic and environmental factors, including mitochondrial DNA (mtDNA) genotype. Previous studies identified mtDNA mutations that are associated with maternally inherited hypertension, including tRNA(Ile) m.4263A>G, m.4291T>C, m.4295A>G, tRNA(Met) m.4435A>G, tRNA(Ala) m.5655A>G, and tRNA(Met)/tRNA(Gln) m.4401A>G, et al. These mtDNA mutations alter tRNA structure, thereby leading to metabolic disorders. Metabolic defects associated with mitochondrial tRNAs affect protein synthesis, cause oxidative phosphorylation defects, reduced ATP synthesis, and increase production of reactive oxygen species. In this review we discuss known mutations of tRNA genes encoded by mtDNA and the potential mechanisms by which these mutations may contribute to hypertension.
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