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. 2020 Jul 24;8:342. doi: 10.3389/fped.2020.00342

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Copyright © 2020 Martinho, Adão, Leite-Moreira and Brás-Silva.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pathogenic mechanisms of persistent pulmonary hypertension of the newborn (PPHN) and its current and potential target therapies: Arachidonic acid-prostacyclin-cAMP pathway. AA, arachidonic acid; AC, adenylyl cyclase; AMP, adenosine monophosphate; cAMP, cyclic adenosine monophosphate; COX, cyclooxygenase; EP, PGE1-receptor; IL-1β, IL-6, IL-8, interleukins-1β, 6 and 8; IP, PGI2-receptor; PDE3, phosphodiesterase-3; PGE1, prostaglandin E1; PGES, PGE1 synthase; PGI2, prostacyclin; PGIS, PGI2 synthase; RV, right ventricle; TBXAS, TXA2 synthase; TNF-α: tumor necrosis factor α; TP, TXA2-receptor; TXA2, thromboxane A2. Target therapies are marked with a syringe icon and are colored based on the type of evidence supporting its use on PPHN- Purple: Evidence on its was obtained by adequately powered RCTs/meta-analysis; Pink: Evidence limited to observational studies or small and underpowered RCTs and/or inconsistent results in human newborns; Blue: Beneficial effects only demonstrated in experimental models of PPHN. This figure was created with BioRender.com.