Activin-A Regulates Bone Morphogenetic Protein Signaling in Pulmonary Endothelial Cells Without Affecting Bone Morphogenetic Protein Type-II Receptor Expression

Pulmonary arterial hypertension (PAH) is a pulmonary disease associated with alterations in gut microbiota. We aimed to identify potential diagnostic genes causally associated with gut microbiota and PAH.

In the recent paper, Pulmonary Vascular Compromise is Associated with Survival in Pediatric Pulmonary Hypertension: a New Computational Model by Niccum et al. [1] presents an innovative computational model reframing pulmonary vascular disease through the concept of pulmonary vascular compromise (PVC), a quantifiable estimate of the proportion of pulmonary vascular surface area lost relative to an idealized normal pulmonary vascular capacity.

Pulmonary arterial hypertension (PAH) is a life-threatening condition with no cure, making research into its underlying mechanisms critical. The platelet-derived growth factor (PDGF) signaling pathway plays a crucial role in vascular remodeling, a key factor in PAH progression. 

Children with single ventricle heart disease (SVHD) demonstrate decreased arginine/NO metabolism following Stage 2 (Glenn) palliation, associated with poor postoperative outcomes. It is unknown if arginine dysregulation persists at Stage 3 (Fontan).