[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]
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