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ABSENCE OF MAST CELLS IN AN EXPERIMENTAL MODEL OF PULMONARY AND CARDIAC FIBROSIS, THE CUX‐1 MICE

Both pulmonary and cardiovascular (CV) fibrosis have a significant role in clinical medicine, however the pathophysiology of fibrosis in these organs is poorly understood (1). Previous rat models of pulmonary fibrosis have shown increased staining of renin and mast cells (MC) production in pulmonary tissue following injection with Triolein (T), a substance comprising 80% of human fat and which is experimentally used to induce fat embolism (FE) (2). MCs are known to produce renin in injured pulmonary tissue, leading to Angiotensin II mediated fibroblasts proliferation (3). The angiotensin II receptor blocker losartan is associated with reduced MCs in fibrotic lungs and a reduction of fibroblasts proliferation, also suggesting that MCs may have a significant correlation with the fibrosis (4).