FGF2 and pulmonary fibrosis: Regarding the mechanisms proposed for the action of hMSCs, Reddy et al. (120) described that the administration of hMSCs down-regulated the expression of both pro-inflammatory cytokines such as IL-2, IL-1β, TNF-α, and TGF-β and pro-fibrotic mediators such as bFGF, CTGF, COL3a1, and CoL1a1, leading to a reduction in inflammation and pulmonary fibrosis.