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This editorial refers to ‘HIF-2α-mediated induction of pulmonary thrombospondin-1 contributes to hypoxia-driven vascular remodelling and vasoconstriction’ by D. Labrousse-Arias et al. , doi:10.1093/cvr/cvv243. In 1971, Baenziger et al. 1 identified a 190 kDa membrane protein in intact platelets that rapidly (within <2 min) disappeared after treatment with thrombin, while a new 107 kDa protein emerged. They concluded that this transition represented hydrolysis of a thrombin-sensitive protein, which likely triggered the physiological effects of thrombin on platelets. Accordingly, the protein was named ‘thrombospondin’ (currently known as thrombospondin-1 or TSP1).2 Since then, TSP1 has emerged as a multifunctional protein playing important roles in numerous physiological and pathological processes, including thrombosis, angiogenesis, tumorigenesis, inflammation, apoptosis, and fibrosis.Recently, TSP1 was linked to pulmonary hypertension (PH), a progressive disease of multiple origins characterized by increased pulmonary artery pressure (>25 mmHg at rest) and extensive lung vascular remodelling that ultimately leads to death due to decompensating right heart failure.3 Despite important advancements in the pharmacotherapy of PH, there is still no cure for this fatal disease. Notably, all of the TSP1 regulated processes listed above, including tumour-like monoclonal proliferation of endothelial cells,4 are implicated in PH pathogenesis. Indeed, the functional role of TSP1 in PH was recently evidenced in independent studies showing partial protection of mice deficient in TSP1 ( tsp1 −/−) from the classic hallmarks of hypoxia-induced PH, i.e. right ventricular pressure elevation …

‘Hypoxio-spondin’: thrombospondin and its emerging role in pulmonary hypertension