Perinatal life is considered a critical time window for determination of long-term metabolic states and organ functions. The perinatal period represents a vulnerable window for the compromised infants

including preterm infants

those who experienced extra-uterine growth restriction (EUGR)

or those otherwise being hospitalized. Molecular and cellular events initiated during this period have the potential to impart lifelong phenotypic changes to infants. This is the basis of the Developmental Origins of Disease Hypothesis. A proposed molecular mechanism by which early events alter later health is epigenetic modifications to chromatin. Epigenetic modifications alter gene expression and subsequently phenotype. One well-studied epigenetic modifier is nutrition

which is important prenatally to the growth and development of the fetus as well as postnatally for preterm infants in the hospital. However

the effects of nutritional disadvantages during perinatal period on pulmonary vascular consequences in later life are not fully understood. Epigenetics plays an important role in the fetal origins of adult diseases. Moreover

endothelial dysfunction is regarded as a precursor of pulmonary arterial hypertension (PAH) and is also related to infant growth. These studies would provide new insights in the prevention and treatment of PAH in childhood or adulthood

and provide a new theoretical basis for controlling the development origin of health and disease

which could have an important clinical significance.