Cited by 629Birth, Development, and HealthEpigenetics and DNA MethylationGenetic Syndromes and Imprinting

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Epigenetic mechanisms that underpin metabolic and cardiovascular diseases

Gluckman, Peter D., Hanson, Mark A., Buklijas, Tatjana, Low, Felicia M., Beedle, Alan S.·2009·Nature Reviews Endocrinology

DOI 10.1038/nrendo.2009.102

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Abstract

Cellular commitment to a specific lineage is controlled by differential silencing of genes, which in turn depends on epigenetic processes such as DNA methylation and histone modification. During early embryogenesis, the mammalian genome is 'wiped clean' of most epigenetic modifications, which are progressively re-established during embryonic development. Thus, the epigenome of each mature cellular lineage carries the record of its developmental history. The subsequent trajectory and pattern of development are also responsive to environmental influences, and such plasticity is likely to have an epigenetic basis. Epigenetic marks may be transmitted across generations, either directly by persisting through meiosis or indirectly through replication in the next generation of the conditions in which the epigenetic change occurred. Developmental plasticity evolved to match an organism to its environment, and a mismatch between the phenotypic outcome of adaptive plasticity and the current environment increases the risk of metabolic and cardiovascular disease. These considerations point to epigenetic processes as a key mechanism that underpins the developmental origins of chronic noncommunicable disease. Here, we review the evidence that environmental influences during mammalian development lead to stable changes in the epigenome that alter the individual's susceptibility to chronic metabolic and cardiovascular disease, and discuss the clinical implications.

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Authors: Gluckman, P. D., Hanson, M. A., Buklijas, T., Low, F. M., & Beedle, A. S.
Affiliations: University of Auckland (NZ)
University of Southampton (GB)
Corresponding author: Gluckman, Peter D.
ORCID: Gluckman, Peter D.
Hanson, Mark A.
Low, Felicia M.
Venue: Nature Reviews Endocrinology
Publisher: Springer Science and Business Media LLC
Published: 2009-06-02
Volume: 5
Issue: 7
Pages: 401-408
ISSN: 1759-5029 (ISSN-L)
1759-5037
DOI: 10.1038/nrendo.2009.102
OpenAlex: W2134682046
Cited by: 627
References: 94
Citations by year: 2026: 14 · 2025: 14 · 2024: 13 · 2023: 26 · 2022: 29 · 2021: 31 · 2020: 37 · 2019: 38 · 2018: 41 · 2017: 43 · 2016: 42 · 2015: 44 · 2014: 49 · 2013: 57 · 2012: 43
FWCI: 6.59
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Endocrinology (publishedVersion)
PubMed (publishedVersion)
ePrints Soton (University of Southampton) (submittedVersion)
ResearchSpace (University of Auckland) (submittedVersion)
Funders: British Heart Foundation
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
Keywords: epigenetics, metabolic disorders, cardiovascular disease, developmental origins of health and disease, DNA methylation, histone modifications, developmental plasticity, transgenerational epigenetic inheritance, gene silencing, non-communicable diseases, disease prevention
MeSH terms: Animals, Cardiovascular Diseases, Humans, Metabolic Diseases, Epigenesis, Genetic

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