CCL2 and pulmonary arterial hypertension: Pulmonary adventitial fibroblasts from a chronic hypoxia model of PAH expressed a persistently pro-inflammatory phenotype, which is defined by a high expression of IL-1β, IL-6, CCL2, CXCL12, CCR7, CXCR4, CD40, CD40L and VCAM-1 [162].