The differentiation of lung fibroblasts into activated myofibroblasts has also been shown to be induced by increased soluble profibrotic factors such as ET-1 and TGF-β1 which are responsible for the production and excessive deposition of EMC characterized by high levels of COL1A, fibronectin, MMP-9, α-SMA and CTGF, molecules involved in ECM remodelling, the progression of the fibrotic process as well as in cardiac hypertrophy [69–73]. This evidence concerns the gene MMP9 and cardiac hypertrophy.