(G) Proposed mechanism. In pulmonary fibrosis, vascular wall thickening is mainly seen in fibrotic areas of the lung; while in PH secondary to PF, vascular remodeling is seen both in fibrotic and non-fibrotic areas of the lung. The extension of vascular wall thickening to the non-fibrotic areas of the lung in PF-PH is concomitant with an increased expression of Slug and PIP in the lungs in both fibrotic and non-fibrotic areas. At the cellular level, Slug up-regulation in macrophages in PF-PH leads to increased PIP expression in the extra-cellular space, which in turn triggers SMC proliferation leading to vascular wall thickening observed in fibrotic and non-fibrotic areas of the lung. (ECM: Extracellular Matrix; SMC / EC : smooth muscle cells and endothelial cells). The number of samples per group for each experiment is included within each bar graph. 