Fig. 1.

Prenatal programming and epigenetics in the genesis of CRS: mechanisms include the heritable changes in gene expression of the cell to its progeny without being encoded into the DNA sequence. Nutrients, oxidative and inflammatory stressors, toxins, and radiation can induce inhibitory or permissive gene expression resulting in chromatin epigenetic remodeling of genes, and ultimately the organism – offspring. Stressors such as excessive or inadequate nutrients (famine) can result in differential gene expression. Dissimilar to genetic changes, epigenetic changes may be more dynamic and reversible, depending on the presence or absence of future inducing factors in the environment. The focus of this image is directed toward cardiovascular and chronic kidney disease. Importantly, there are other clinical abnormalities such as: hypertension, obesity, insulin resistance, non-alcoholic fatty liver disease, and type 2 diabetes mellitus. ER = Endoplasmic reticulum; FFA = free fatty acids; IR = insulin resistance; NO = nitric oxide; NOO^– = peroxynitrite; PAI-1 = plasminogen activator inhibitor; ROS = reactive oxygen species; TNF = tumor necrosis factor; TPA = tissue plasminogen activator; # = number.