Klotho and Renal Fibrosis

Renal fibrosis is a pathological condition that characterized by excessive accumulation of extracellular matrix (ECM) and it is a common pathway of progression in different renal diseases including chronic glomerulonephritis, diabetic nephropathy chronic allograft nephropathy and renal senescence (1, 2). In the process of renal fibrosis leukocyte infiltration, activation of fibroblasts and myofibroblasts, epithelial-mesenchymal transition (EMT) all have been identified as the major events (3). Behind The pathological features there are complex orchestrated interplay of different factors including cytokines (TGF-β, IFN-γ, IL-10), transcriptional activator factors (Sp1, Egr-1, Smad3), cell surface repressors down regulation or up regulation (Smad7, Fli-1, PPAR-γ, p53, Klotho) and epigenetic modulators (acetyltransferase, methyltransferases, deacetylases, microRNAs) (4). Deregulation of pro-fibrotic and down regulation of anti-fibrotic factors play an important role in initiation and progression of renal fibrosis. Understanding the mechanism would be valuable to diagnose, prevent and even reverse the process of fibrosis. The role of micro RNA as a biomarker or as a therapeutic modality of renal fibrosis has recently be discussed by authors (5).