Key result
This review highlights the role of cortical actin architecture, primarily γ-actin, in the transduction of mechanical force in the hypoxic pulmonary circuit of persistent pulmonary hypertension of the newborn.
This review highlights the critical role of actin polymerization and cytoskeletal remodeling, particularly γ-actin, in the pathophysiology of persistent pulmonary hypertension of the newborn.
Hypothesis-generating for cytoskeletal targets in PPHN; leaves open whether γ-actin modulation improves newborn outcomes.
Persistent pulmonary hypertension of the newborn (PPHN) is defined as the failure of normal pulmonary vascular relaxation at birth. Hypoxia is known to impede postnatal disassembly of the actin cytoskeleton in pulmonary arterial myocytes, resulting in elevation of smooth muscle α-actin and γ-actin content in elastic and resistance pulmonary arteries in PPHN compared with age-matched controls. This review examines the original histological characterization of PPHN with attention to cytoskeletal structural remodeling and actin isoform abundance, reviews the existing evidence for understanding the biophysical and biochemical forces at play during neonatal circulatory transition, and specifically addresses the role of the cortical actin architecture, primarily identified as γ-actin, in the transduction of mechanical force in the hypoxic PPHN pulmonary circuit.
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Fediuk et al. (2015) conducted a review in Persistent pulmonary hypertension of the newborn (PPHN). Actin polymerization and cortical actin architecture was evaluated. This review highlights the role of cortical actin architecture, primarily γ-actin, in the transduction of mechanical force in the hypoxic pulmonary circuit of persistent pulmonary hypertension of the newborn.
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