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Essential hypertension (EH) is an escalating problem for developed and developing countries. It is currently seen as a ’complex’ genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions. Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement. However, the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in essential hypertension still remains perplexing. With the application of a variety of imaging approaches and successive mouse model of mitochondrial diseases we convince that these problems will be resolved in the near future.
Essential hypertension (EH) is an escalating problem for developed and developing countries. It is currently seen as a ’complex’ genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions. Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement. However, the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in With the application of a variety of imaging approaches and successive mouse model of mitochondrial diseases we convince that these problems will be resolved in the near future.