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Renal fibrosis is widely regarded as a common pathway contributing to end-stage renal disease, characterized by aberrant activation and the development of renal fibroblasts and overproduction of proteins of extracellular matrix (ECM) (Meng et al. 2014). During fibrosis, the kidney is stimulated by various pathogenic factors in diverse diseases including trauma, infection, inflammation, blood circulation disorder, and immune response. Fibrosis can be viewed as an aberrant wound healing, in which there is progression rather than scar recovery following damage, and fibroblasts are central to this process. Fibrosis is closely related to tissue regeneration and inflammation, which is mediated by specific types of cells, including epithelial, endothelial, fibroblast, pericyte, myofibroblast, and inflammatory cells (Duffield 2014). Pathogenic factors such as drug poisoning, high blood pressure, diabetes, and infection can cause damage to the intrinsic cells which can release some cytokines.
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