Transgenerational Epigenetic Inheritance of Cardiovascular Diseases: A Network Medicine Perspective

Introduction The ability to identify early epigenetic signatures underlying the inheritance of cardiovascular risk, including trans- and intergenerational effects, may help to stratify people before cardiac symptoms occur. Methods Prospective and retrospective cohorts and case–control studies focusing on DNA methylation and maternal/paternal effects were searched in Pubmed from 1997 to 2023 by using the following keywords: DNA methylation, genomic imprinting, and network analysis in combination with transgenerational/intergenerational effects. Results Maternal and paternal exposures to traditional cardiovascular risk factors during critical temporal windows, including the preconceptional period or early pregnancy, may perturb the plasticity of the epigenome (mainly DNA methylation) of the developing fetus especially at imprinted loci, such as the insulin-like growth factor type 2 (IGF2) gene. Thus, the epigenome is akin to a “molecular archive” able to memorize parental environmental insults and predispose an individual to cardiovascular diseases onset in later life. Direct evidence for human transgenerational epigenetic inheritance (at least three generations) of cardiovascular risk is lacking but it is supported by epidemiological studies. Several blood-based association studies showed potential intergenerational epigenetic effects (single-generation studies) which may mediate the transmittance of cardiovascular risk from parents to offspring. Discussion In this narrative review, we discuss some relevant examples of trans- and intergenerational epigenetic associations with cardiovascular risk. In our perspective, we propose three network-oriented approaches which may help to clarify the unsolved issues regarding transgenerational epigenetic inheritance of cardiovascular risk and provide potential early biomarkers for primary prevention..

What is already known on this subject? Many maternal risk factors, including dyslipidemia, hypertension, smoking, diabetes, and obesity have been associated with CVDs risk in the offspring. Paternal factors are emerging as risk factors contributing to transgenerational effects. From a molecular point of view, DNA methylation may be responsible, at least in part, for early modifications during fetal development which set CVD risk trajectories during post-natal life. What this study adds? Big data availability supports the importance of Network Medicine approaches for integrating environmental exposures, clinical information, and advanced next-generation sequencing platform data over time, representing one of the most potent research paradigms for identifying novel molecular routes underlying the potential transmittance of CVD risk from parents to their offspring. The possible inheritance of DNA methylation signatures from parents to offspring and the ability to detect them using cardiac tissue, or blood as surrogate, may provide useful biomarkers for primary prevention of CVDs..

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:28

Enthalten in:

Maternal and child health journal - 28(2024), 4 vom: 26. Feb., Seite 617-630

Sprache:

Englisch

Beteiligte Personen:

Benincasa, Giuditta [VerfasserIn]
Napoli, Claudio [VerfasserIn]
DeMeo, Dawn L. [VerfasserIn]

Links:

Volltext [lizenzpflichtig]

BKL:

44.67

Themen:

Cardiovascular risk
Epigenetic inheritance
Intergenerational effects
Network medicine
Primary prevention
Transgenerational effects

Anmerkungen:

© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

doi:

10.1007/s10995-023-03886-z

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

SPR055287409