title: Maternal-foetal epigenetic interactions in the beginning of cardiovascular damage.
abstract: Several studies indicate that impaired foetal growth, and in utero exposure to risk factors, especially maternal hypercholesterolaemia, may be relevant for the early onset of cardiovascular damage. The exact molecular mechanisms of such foetal programming are still unclear. Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of cardiovascular disease (CVD) during adulthood. Translational studies support this hypothesis; however, a direct causality in humans has not been ascertained. This hypothesis could be investigated in primates and in human post-mortem foetal arteries. Importantly, some studies also suggest the transgenerational transmission of epigenetic risk. The recently launched International Human Epigenome Consortium and the NIH Roadmap Epigenomics Mapping Consortium will provide the rationale for a useful clinical scenario for primary prevention and therapy of CVD. Despite the heritable nature of epigenetic modification, the clinically relevant information shows that it could be reversible through therapeutic approaches, including histone deacetylase inhibitors, histone acetyltransferase inhibitors, and commonly used drugs such as statins.
authors.affiliation: Department of General Pathology, Division of Clinical Pathology and Excellence Research Centre on Cardiovascular Disease, U.O.C. Division of Immunohematology and Transplantation-CRT, 1st School of Medicine, Complesso S. Andrea delle Dame, Second University of Naples, 80138 Naples, Italy. claudio.napoli@unina2.it
authors.forename: Claudio
authors.initials: C
authors.lastname: Napoli
authors.forename: Teresa
authors.initials: T
authors.lastname: Infante
authors.forename: Amelia
authors.initials: A
authors.lastname: Casamassimi
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000196:embryology / Q000235:genetics* / Q000517:prevention & control; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D020022:Genetic Predisposition to Disease; D040941:Heredity; D006801:Humans; D011247:Pregnancy; D011322:Primary Prevention; D018570:Risk Assessment; D012307:Risk Factors