Abstract
Genetic and environmental agents that disrupt organogenesis are numerous and well described. Less well established, however, is the role of delay in the developmental processes that yield functionally immature tissues at birth. Evidence is mounting that organs do not continue to develop postnatally in the context of these organogenesis insults, condemning the patient to utilize under-developed tissues for adult processes. These poorly differentiated organs may appear histologically normal at birth but with age may deteriorate revealing progressive or adult-onset pathology. The genetic and molecular underpinning of the proposed paradigm reveals the need for a comprehensive systems biology approach to evaluate the role of maternal-fetal environment on organogenesis.You may delay, but time will notBenjamin FranklinUSA Founding Father
Highlights
The fragility of the developmental process is well known with estimates as high as 70% of conceptions lost in early pregnancy [1]
What are diseases of organogenesis that result from developmental delay and not disruption called? In premature infants terms like fetal and immature are used to describe their gestational correct, underdeveloped organs
We propose that the temporal state of many tissues can become fixed at birth, resulting in organs that are functionally immature
Summary
The fragility of the developmental process is well known with estimates as high as 70% of conceptions lost in early pregnancy [1]. The obvious immediate consequences seen in any neonatal unit include poor lung function, intestinal deficiencies, immune system deficiencies, and poor renal function These immediate problems combined with therapies used to combat them can lead to significant morbidity and mortality in the premature infant. The epidemiologic basis for late or adult-onset diseases, following either premature birth or low birth weight, includes poor pre-natal maternal nutrition and smoking during pregnancy both of which are reviewed previously [11,12]. These epidemiologic correlations do no provide a theoretical, molecular basis for explaining late onset of diseases related to delays in organogenesis.
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