Abstract
Renal fibrosis is the common pathway for progression of chronic kidney disease (CKD) to end stage of renal disease. It is now widely accepted that the degree of renal fibrosis correlates with kidney function and CKD stages. The key cellular basis of renal fibrosis includes activation of myofibroblasts, excessive production of extracellular matrix components, and infiltration of inflammatory cells. Many cellular mechanisms responsible for renal fibrosis have been identified, and some antifibrotic agents show a greater promise in slowing down and even reversing fibrosis in animal models; however, translating basic findings into effective antifibrotic therapies in human has been limited. In this chapter, we will discuss the effects and mechanisms of some novel antifibrotic agents in both preclinical studies and clinical trials.
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