The pathogenesis of fibrotic disorders is similar regardless of the ti
ssues involved. Inflammatory leukocytes infiltrate the site triggered
by chemotactic and activating mediators. This is followed by the elabo
ration of cytokines that directly and indirectly induce the proliferat
ion of fibroblasts and endothelial cells and the deposition of extrace
llular matrix (ECM). In the absence of inhibitory signals, the continu
ed production of these mediators sustains the connective tissue accumu
lation, which results in permanent alteration in tissue structure and
function.