In the present study, by using a novel canine model, we uncovered several primary findings: (i) OSA aggravated pulmonary fibrosis as well as bronchial and vascular remodeling without causing obvious pulmonary hypertension, (ii) OSA enhanced local sympathetic sprouting and changed the expression and distribution of nerve fibers via promoting the expression of TH, GAP43 and NGF, (iii)besides the hyperactivation TGF-β/Smad2 pathway, ERK, CaMK II and PKC δ mediated pathways were also possibly participating in the OSA induced pulmonary remodeling. The gene discussed is TGFB1; the disease is pulmonary fibrosis.