Mitochondrial tRNA Mutations Associated With Essential Hypertension: From Molecular Genetics to Function

Yuqi Liu; Yundai Chen

doi:10.3389/fcell.2020.634137

Mitochondrial tRNA Mutations Associated With Essential Hypertension: From Molecular Genetics to Function

Front Cell Dev Biol. 2021 Jan 22:8:634137. doi: 10.3389/fcell.2020.634137. eCollection 2020.

Authors

Yuqi Liu^{1

2

3

4}, Yundai Chen⁵

Affiliations

¹ Cardiac Department, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China.
² Department of Cardiology & National Clinical Research Center of Geriatrics Disease, Chinese PLA General Hospital, Beijing, China.
³ Beijing Key Laboratory of Chronic Heart Failure Precision Medicine, Chinese PLA General Hospital, Beijing, China.
⁴ National Key Laboratory of Kidney Diseases, Chinese PLA General Hospital, Beijing, China.
⁵ Cardiac Department, Chinese PLA General Hospital, Beijing, China.

Abstract

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.

Keywords: hypertension; maternal; mtDNA; mutation; tRNA.

Publication types

Review
Retracted Publication