Renal fibrosis is the final common pathway for nearly all forms of kidney disease that progress towards end-stage renal failure. As a sequel of inflammation and injury, humoral factors are released by infiltrating and resident renal cells that stimulate kidney tissues to produce extracellular matrix (ECM) molecules, like type I and III collagens, fibronectin and proteoglycans [1, 2]. It is believed that overproduction of such ECM generates fibrosis, leading to the permanent loss of normal structure and function in the kidney [1, 2]. Thus, to understand chronic progressive renal disease as a whole, and to develop specific therapy, it is absolutely necessary to better clarify the mechanisms of renal fibrosis. Since dealing with all aspects of renal fibrosis is beyond the scope of this article, we will review common mechanisms using recent data, and then focus on the biology of fibroblasts, one of the pivotal participants in tissue fibrosis.