The pathogenesis of progressive chronic renal disease and therapeutic strategies, based on the axis of macrophages and myofibroblasts

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Fibrosis is developed after tissue injury. Regardless etiology,interstitial fibrosis occurs after renal injury, then leading to chronic kidney disease.The properties of macrophages and myofibroblasts, both which play central roles in fibrosis, were investigated using cisplatin-induced rat renal failure model. CD68 macrophages appeared at early stages, whereas at the advanced stages, MHC class II-expressing macrophages and lymphocytes appeared. Besides epithelial-mesenchymal transition (EMT), myofibroblasts may be derived from mesenchymal cells such as medullary interstitial cells and pericytes in lineage of stem cells. EMT phenomenon was seen exclusively in abnormally regenerating renal epithelia; the formation is inhibited by PGE2 but promoted by osteopontin. Characteristics of hepatic, pulomonary and cutaneous fibrosis were investigated as well. Clarifying the pathogenesis of fibrosis could lead to exploration of possible therapies.