Mitochondrial DNA mutations and essential hypertension (Review).

摘要: Essential hypertension (EH) is a frequent, chronic, age-related disorder, which remains major modifiable risk factor for cardiovascular disease despite important advances in our understanding of its pathophysiology. Previous studies have noted consistent maternal effect on blood pressure (BP). Consequently, mutations mitochondrial DNA (mtDNA) become an additional target investigations the missing BP heritability. Among these mutations, mt-transfer RNA (tRNA) hot mutational spot pathogenic associated with EH. Mutant mtDNA aggravates dysfunction, pivotally contributing to clinical phenotype. Moreover, damaged mitochondria, due their inability provide high-energy requirements cells, generate reactive oxygen species (ROS) and induce mitochondrial-mediated cell death pathways. Therefore, dysfunction plays critical role pathogenesis This review summarizes basic knowledge genetics EH-associated further discusses molecular mechanisms behind manifestations