期刊
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
卷 43, 期 -, 页码 85-95出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2015.06.006
关键词
Intergenerational epigenetic inheritance; Developmental programming; Maternal obesity; Intrauterine growth restriction; Maternal protein restriction; Global nutrient restriction; Methylation; Histone modifications; Chromatin; MicroRNAs; piRNAs
资金
- MRC Metabolic Diseases Unit award [MC_UU_12012/4]
- Biotechnology and Biological Sciences Research Council [BB/D01235X/1, BB/D01235X/2] Funding Source: researchfish
- British Heart Foundation [FS/09/029/27902] Funding Source: researchfish
- Medical Research Council [MR/J001562/1, MC_UU_12012/4, MC_UU_12012/5, MC_UU_12012/5/B] Funding Source: researchfish
- BBSRC [BB/D01235X/1, BB/D01235X/2] Funding Source: UKRI
- MRC [MR/J001562/1, MC_UU_12012/4] Funding Source: UKRI
It is now well established that the environment to which we are exposed during fetal and neonatal life can have a long-term impact on our health. This has been termed the developmental origins of health and disease. Factors known to have such programming effects include intrauterine nutrient availability (determined by maternal nutrition and placental function), endocrine disruptors, toxins and infectious agents. Epigenetic processes have emerged as a key mechanism by which the early environment can permanently influence cell function and metabolism after multiple rounds of cell division. More recently it has been suggested that programmed effects can be observed beyond the first generation and that therefore epigenetic mechanisms could form the basis of transmission of phenotype from parent to child to grandchild and beyond. Here we review the evidence for such processes. (C) 2015 Published by Elsevier Ltd.
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