Abstract
Preterm birth (< 37 gestational weeks) reaches 10% of total births worldwide. Early exposure to an ex utero environment can alter organogenesis and maturation in the newborn. This early onset of events can further promote long-term developmental alterations and cardiovascular disease risks. Mechanisms activated during preterm birth and promoting such cardiovascular alterations have just recently been investigated. As a major candidate, the renin angiotensin aldosterone system (RAAS) can be acutely altered during preterm birth and persistently activated in later life. Further, RAAS alterations may occur as consequence of kidney and heart immaturity to promote adaptive responses, suggesting a dual role of this system on fetal and neonatal organogenesis. Furthermore, fetal or neonatal exposure to deleterious stress conditions can significantly impact on this dual RAAS role, contributing to the establishment of hemodynamic and structural alterations. In this review, clinical and experimental findings describing RAAS components and activation in relationship with preterm birth are discussed. Further clinical and experimental investigations on RAAS activation in the context of preterm birth are needed to better understand this dual role of RAAS on early development and on programming of risks to cardiovascular diseases.
Keywords: Preterm birth, renin angiotensin aldosterone system, cardiovascular diseases, pregnancy complications, neonatal complications.
Graphical Abstract
Related Journals
Current Protein & Peptide Science
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Frontiers in Protein and Peptide Sciences
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