With the increasing incidence of chronic renal diseases worldwide, there is an urgent need to understand the mechanisms involved in progression of renalfibrosis. Independently of the underlying cause or trigger, progression of renalfibrosis is mainly characterized by excessive synthesis and abnormal accumulation of extracellular matrix proteins in renal mesenchymal cells. These cells are mainly myofibroblasts deriving from phenotypic transformation of a variety of renal cells, including vascular smooth muscle cells, mesangial cells, tubular epithelial cells, endothelial cells, and pericytes. Recent animal studies showing the regression of renal fibrosis during curative therapy suggest that this phenotypic "transition" is reversible. The plasticity of podocytes controlling glomerular filtration may also play a role in the progression/regression of fibrosis in this setting