Background and Aims: we previously reported in studies on organoid-cultured bovine pulmonary arteries that pulmonary hypertension (PH) conditions of exposure to hypoxia or endothelin-1 caused a loss of a cartilage oligomeric matrix protein (COMP) stabilization of bone morphogenetic protein receptor-2 (BMPR2) function, a known key process contributing to pulmonary hypertension development. This evidence concerns the gene BMPR2 and pulmonary arterial hypertension.