Abstract
End-stage renal disease is continuously rising worldwide. Over the last decade, the characterization of mediators of progression and targets for therapy of chronic kidney disease have been challenging for the scientific community. In renal diseases, independently of the initiating cause, the main structural alterations derive from the expansion of renal fibrosis, which results from the impairment of a regulated balance between pro- and antifibrotic factors. In this chapter, we discuss the role of the major factors that promote renal fibrosis, both in experimental models and human diseases, as well as different therapeutic concepts to inhibit or reverse chronic renal disease. We also discuss the pathological roles of three new potential mediators of renal disease—DDR-1, periostin, and connexin 43—which may be considered as major targets for antifibrotic drugs to be introduced to clinical use.
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