Metabolic and adult-onset diseases arise at the confluence of genetics and environmental factors. However, genetic and postnatal environmental exposures cannot fully explain the distressing rise in disease prevalence. Strong evidence supports the notion that many adult-onset diseases are linked to early exposures (preconception as well as in utero). Prenatal development is a period of rapid growth and cell differentiation; hence, epigenomic alterations during this period make individuals particularly vulnerable to adverse conditions with significant impact on organ structure, function, and propensity for clinically defined diseases later in life. Therefore, epigenetics remodeling may serve as biological memory of early life exposures, with resulting shifts in gene regulatory marks affecting long-term cellular identity, function, and cell fate.
Recent findings in epigenetics significantly help us to advance our understanding of mechanisms involved in age-related and metabolic diseases’ developmental programming. Thus, our ability to further explore epigenetics in its full complexity and at a higher resolution through integrative models is instrumental to providing new insights in developmental programming of adult diseases.
This Research Topic welcomes Original Research, Methods, Commentaries, Perspectives, and Reviews on the state-of-the-art research and the future directions for early epigenetics influences on later life metabolic diseases. Specifically, we encourage the submission related to the following (but not limited to) topics:
• How epigenetic cellular memory and cellular plasticity participate in metabolic and later life diseases.
• Multigenerational and transgenerational epigenetic inheritance, including both maternal and paternal transmission, on later life and metabolic diseases onset and evolution.
• Stem cell epigenetic therapy applied to metabolic and later life diseases.
• Advances in integrative and bioinformatic analysis of epigenetic data.
• Epigenetics in the midst of single-cell technology.
• Epigenetics and sexual dimorphism effects on metabolic and later life diseases.
Metabolic and adult-onset diseases arise at the confluence of genetics and environmental factors. However, genetic and postnatal environmental exposures cannot fully explain the distressing rise in disease prevalence. Strong evidence supports the notion that many adult-onset diseases are linked to early exposures (preconception as well as in utero). Prenatal development is a period of rapid growth and cell differentiation; hence, epigenomic alterations during this period make individuals particularly vulnerable to adverse conditions with significant impact on organ structure, function, and propensity for clinically defined diseases later in life. Therefore, epigenetics remodeling may serve as biological memory of early life exposures, with resulting shifts in gene regulatory marks affecting long-term cellular identity, function, and cell fate.
Recent findings in epigenetics significantly help us to advance our understanding of mechanisms involved in age-related and metabolic diseases’ developmental programming. Thus, our ability to further explore epigenetics in its full complexity and at a higher resolution through integrative models is instrumental to providing new insights in developmental programming of adult diseases.
This Research Topic welcomes Original Research, Methods, Commentaries, Perspectives, and Reviews on the state-of-the-art research and the future directions for early epigenetics influences on later life metabolic diseases. Specifically, we encourage the submission related to the following (but not limited to) topics:
• How epigenetic cellular memory and cellular plasticity participate in metabolic and later life diseases.
• Multigenerational and transgenerational epigenetic inheritance, including both maternal and paternal transmission, on later life and metabolic diseases onset and evolution.
• Stem cell epigenetic therapy applied to metabolic and later life diseases.
• Advances in integrative and bioinformatic analysis of epigenetic data.
• Epigenetics in the midst of single-cell technology.
• Epigenetics and sexual dimorphism effects on metabolic and later life diseases.
