title: Fetal programming and epigenetic mechanisms in arterial hypertension.
abstract: OBJECTIVE
  To provide an overview of available evidence of the potential role of epigenetics in the pathogenesis of hypertension and vascular dysfunction.
  
  
  RESULTS
  Arterial hypertension is a highly heritable condition. Surprisingly, however, genetic variants only explain a tiny fraction of the phenotypic variation and the term 'missing heritability' has been coined to describe this phenomenon. Recent evidence suggests that phenotypic alteration that is unrelated to changes in DNA sequence (thereby escaping detection by classic genetic methodology) offers a potential explanation. Here, we present some basic information on epigenetics and review recent work consistent with the hypothesis of epigenetically induced arterial hypertension.
  
  
  CONCLUSIONS
  New technologies that enable the rigorous assessment of epigenetic changes and their phenotypic consequences may provide the basis for explaining the missing heritability of arterial hypertension and offer new possibilities for treatment and/or prevention.
authors.affiliation: aDepartment of Cardiology and Clinical Research, Inselspital, University Hospital Bern, Bern, Switzerland bFacultad de Ciencias, Departamento de Biología, Universidad de Tarapacá, Arica, Chile cDepartment of Internal Medicine, University Hospital, Lausanne, Switzerland dMount Sinai Health Medical Center, Icahn School of Medicine, Division of Cardiology, New York, USA *Emrush Rexhaj and Urs Scherrer contributed equally to the writing of this article.
authors.forename: Urs
authors.initials: U
authors.lastname: Scherrer
authors.forename: Stefano F
authors.initials: SF
authors.lastname: Rimoldi
authors.forename: Claudio
authors.initials: C
authors.lastname: Sartori
authors.forename: Franz H
authors.initials: FH
authors.lastname: Messerli
authors.forename: Emrush
authors.initials: E
authors.lastname: Rexhaj
mesh_terms: D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D011247:Pregnancy