Figure 1.

P-selectin in pulmonary artery smooth muscle cells (PASMCs) contributes to the pathophysiology of pulmonary hypertension. Novoyatleva and colleagues (8) show that hypoxia upregulates P-selectin in PASMCs in a HIF-1α (hypoxia-induced factor-1α)-dependent manner. P-selectin–dependent activation of NF-κB (nuclear factor-κB), Akt–mTOR (mammalian target of rapamycin)–p70S6K (p70 ribosomal S6 kinase), ERK (extracellular signal–regulated kinase), and p38 signaling pathways in PASMCs contribute to PASMC proliferation and vascular remodeling, which is reversed by the P-selectin inhibitor fucoidan. Illustration by Jacqueline Schaffer.