Essential Hypertension May Be Maternally Inherited(41828)

April 1, 2011

Hypertension is a major public health problem affecting billions worldwide. The latest research found that essential hypertension may be maternally inherited. The research team headed by Prof. Guan Minxin at College of Life Sciences, Zhejiang University, Prof. Wang Shiwen at Chinese PLA General Hospital and faculty of Cincinnati Children s Hospital and Medical University of Vienna collaborated in conducting a research to understand the pathogenesis of maternally inherited hypertension related to mitochondrial dysfunction.

Experts believe that the study for the first time establishes the causal link between mitochondrial dysfunction and essential hypertension, which helps to provide new theoretical bases for early diagnosis, intervention and prevention of hypertension.

From 2006, the research team led by Prof. Wang Shiwen investigated a family with essential hypertension and found that the essential hypertension of this family carried typical maternal genetic characteristics. In this family, a total of 106 subjects underwent clinical, genetic, molecular, and biochemical evaluations.

Fifteen of 24 adult matrilineal relatives exhibited a wide range of severity in essential hypertension, whereas none of the offspring of affected fathers had hypertension. This observation prompted scientists to speculate that essential hypertension may be associated with mitochondrial dysfunction.

Mitochondria are organelles whose job is to generate power for cells. Only mothers mitochondrial DNA can be passed to the next generation, i. e., the mitochondrial genetic characteristics and mitochondrial diseases such as Leber s hereditary optic neuropathy and Kearns-Sayre syndrome are all maternally inherited. Prof. Guan Minxin specializes in the study of mitochondrial diseases and is committed to finding the disease-causing culprit in the mitochondrial gene of the family.

Mutational analysis of the mitochondrial genome done by Prof. Guan s research team has identified the novel 4263A>G mutation in this Chinese family. It is anticipated that the 4263A>G mutation leads to the reduced rate of mitochondrial protein synthesis, which appears to be responsible for the reduced activities of the mitochondrial respiration chain. Subsequently, these defects result in the reduction of ATP production and an increase of reactive oxygen species production. These mitochondrial dysfunctions may contribute to the development of hypertension.

The study was published on the latest issue of Circulation Research, a top journal in the field of Cardiovascular research.

Essential Hypertension May Be Maternally Inherited

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