Abstract
Research in the role of cytokines in experimental glomerulonephritis has increased our understanding of the mechanisms that may be involved in the development of progressive renal disease. Glomerulosclerosis, the final common pathway in a variety of underlying kidney diseases, is characterized by increased extracellular matrix formation and cell proliferation. Transforming growth factor-beta (TGF-beta) and monocyte chemoattractant protein-1 (MCP-1) have been identified in animal models as mediators in the processes that follow renal injury. There is evidence of similar events occurring in other fibrotic disorders, suggesting that there is a common generic pathway of fibrosis. This review summarizes our knowledge of TGF-beta and MCP-1 in experimental kidney disease and compares these results with mechanisms described in other organs. We propose that glomerulosclerosis represents Defektheilung (healing by secondary intention) of the kidney after various injuries. The growing knowledge of the mechanisms involved will help advance future therapeutic interventions by directing the healing process toward primary healing.
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