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Epigenetic mechanisms that underpin metabolic and cardiovascular diseases
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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“Epigenetic changes such a DNA methylation and histone modification may be transmitted across generations either directly by persisting through meiosis or indirectly through replication in the next generation of the environmental conditions in which the epigenetic change occurred 46, 49.”
From The Circadian Syndrome: is the Metabolic Syndrome and much more! (2019) · cites this paper as [46]
In the citing paper
“This underlines that epigenetic processes are a key mechanism that alter the individual's susceptibility to the development of NCDs like T2DM and CVD 46, 50.”
From The Circadian Syndrome: is the Metabolic Syndrome and much more! (2019) · cites this paper as [46]
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Metadata
- 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.
- Venue
- Nature Reviews Endocrinology
- Published
- 2009-06-02
- Volume
- 5
- Issue
- 7
- Pages
- 401-408
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- 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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