The concept that early life stressors can program later chronic disease was first proposed by David Barker in the 1980s and is investigated in the field of Developmental Origins of Health and Disease (DOHaD). Environmental exposure to toxicants, hormones, and malnutrition during critical developmental stages (preconception, gestation, lactation, puberty, and young adulthood) deregulate development, influencing long-term control of tissue physiology, and homeostasis. Particularly during early life epigenetic marks (DNA methylation, histone post-translational modifications, and microRNA expression) highly plastic during early life and susceptible to environmental deregulation. Thus, epigenetic represents a promising underlying mechanism of developmental programming. A better understanding of the epigenetic markers in the DOHaD context is fundamental to the establishment of better intervention strategies for chronic disease prevention, starting very early in life.
Given that multiple mechanisms have been proposed to underlie developmental programming, especially epigenetic, but also organ structure alterations, deregulation of stem cell function, and accelerated aging, multidisciplinary scientific perspectives (cellular and developmental biology, biochemistry, molecular biology, physiology, toxicology, nutrition, among others) are needed to attain this concept. Better elucidation of cellular and developmental biology aspects involved in DOHaD holds promise to establish innovative chronic disease prevention strategies that would start from early life.
This current Research Topic aims to cover recent and novel research trends in cellular and developmental biology aspects related to DOHaD, with an emphasis on epigenetic deregulation in cell proliferation and differentiation, metabolism, stem cell function, among other processes.
We aim to cover promising, recent, and novel research trends in cellular and developmental biology related to epigenetic developmental programming. Research involving basic, translational, and clinical data, as well as systematic review and meta-analysis, will be organized to publish novel contributions and breaking results on all aspects of the DOHaD concept. Areas to be covered in this Research Topic may include, but are not limited to epigenetic aspects of:
? Early life exposures (such as toxicants, drugs, hormones, nutrition, stress, infections, physical activity) and developmental programming of obesity, type 2 diabetes, cardiovascular diseases, cancer, aging among others.
? Maternal exposures during preconception, gestation and lactation and effects on developmental programming
? Paternal exposures during preconception and developmental programming
? Exposures during childhood, puberty and early adulthood and developmental programming
? Transgenerational developmental programming
? Stem cells and developmental programming
The concept that early life stressors can program later chronic disease was first proposed by David Barker in the 1980s and is investigated in the field of Developmental Origins of Health and Disease (DOHaD). Environmental exposure to toxicants, hormones, and malnutrition during critical developmental stages (preconception, gestation, lactation, puberty, and young adulthood) deregulate development, influencing long-term control of tissue physiology, and homeostasis. Particularly during early life epigenetic marks (DNA methylation, histone post-translational modifications, and microRNA expression) highly plastic during early life and susceptible to environmental deregulation. Thus, epigenetic represents a promising underlying mechanism of developmental programming. A better understanding of the epigenetic markers in the DOHaD context is fundamental to the establishment of better intervention strategies for chronic disease prevention, starting very early in life.
Given that multiple mechanisms have been proposed to underlie developmental programming, especially epigenetic, but also organ structure alterations, deregulation of stem cell function, and accelerated aging, multidisciplinary scientific perspectives (cellular and developmental biology, biochemistry, molecular biology, physiology, toxicology, nutrition, among others) are needed to attain this concept. Better elucidation of cellular and developmental biology aspects involved in DOHaD holds promise to establish innovative chronic disease prevention strategies that would start from early life.
This current Research Topic aims to cover recent and novel research trends in cellular and developmental biology aspects related to DOHaD, with an emphasis on epigenetic deregulation in cell proliferation and differentiation, metabolism, stem cell function, among other processes.
We aim to cover promising, recent, and novel research trends in cellular and developmental biology related to epigenetic developmental programming. Research involving basic, translational, and clinical data, as well as systematic review and meta-analysis, will be organized to publish novel contributions and breaking results on all aspects of the DOHaD concept. Areas to be covered in this Research Topic may include, but are not limited to epigenetic aspects of:
? Early life exposures (such as toxicants, drugs, hormones, nutrition, stress, infections, physical activity) and developmental programming of obesity, type 2 diabetes, cardiovascular diseases, cancer, aging among others.
? Maternal exposures during preconception, gestation and lactation and effects on developmental programming
? Paternal exposures during preconception and developmental programming
? Exposures during childhood, puberty and early adulthood and developmental programming
? Transgenerational developmental programming
? Stem cells and developmental programming
