TY - JOUR
T1 - Epigenetic basis for fetal origins of age-related disease
AU - Thompson, Reid F.
AU - Einstein, Francine H.
PY - 2010/3/1
Y1 - 2010/3/1
N2 - The current concept of fetal origins of adult diseases describes in utero programming, or adaptation to a spectrum of adverse environmental conditions that ultimately leads to increased susceptibility to age-related diseases (e.g., type 2 diabetes and cardiovascular disease) later in life. Although the precise mechanism of this biological memory remains unclear, mounting evidence suggests an epigenetic basis. The increased susceptibility to chronic disease and involvement of multiple organ systems that is observed is analogous to the decline in resistance to disease that is typical of normal aging. Although the cumulative environment over the course of a lifetime can induce increasing epigenetic dysregulation, we propose that adverse events that occur during early development can induce significant additional dysregulation of the epigenome. Here, we describe the current evidence for fetal origins of adult disease and the associated role of epigenetic dysregulation. In addition, we present a new perspective on the induction of epigenetic alterations in utero, which subsequently lead to an aging phenotype marked by increased susceptibility to age-related diseases.
AB - The current concept of fetal origins of adult diseases describes in utero programming, or adaptation to a spectrum of adverse environmental conditions that ultimately leads to increased susceptibility to age-related diseases (e.g., type 2 diabetes and cardiovascular disease) later in life. Although the precise mechanism of this biological memory remains unclear, mounting evidence suggests an epigenetic basis. The increased susceptibility to chronic disease and involvement of multiple organ systems that is observed is analogous to the decline in resistance to disease that is typical of normal aging. Although the cumulative environment over the course of a lifetime can induce increasing epigenetic dysregulation, we propose that adverse events that occur during early development can induce significant additional dysregulation of the epigenome. Here, we describe the current evidence for fetal origins of adult disease and the associated role of epigenetic dysregulation. In addition, we present a new perspective on the induction of epigenetic alterations in utero, which subsequently lead to an aging phenotype marked by increased susceptibility to age-related diseases.
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U2 - 10.1089/jwh.2009.1408
DO - 10.1089/jwh.2009.1408
M3 - Review article
C2 - 20136551
AN - SCOPUS:77950229907
SN - 1540-9996
VL - 19
SP - 581
EP - 587
JO - Journal of Women's Health
JF - Journal of Women's Health
IS - 3
ER -