Activated Pericytes and the Inhibition of Renal Vascular Stability

Abstract

The hallmark feature of CKD and its progression to end stage is the presence and severity of interstitial fibrosis.1,2 This long-recognized association is the prime driving force of research to understand the nature of renal scarification. Much of the research in this area can be grouped into one of two broad categories: efforts geared toward understanding the biochemical and pathophysiological factors that govern the degree of progression and efforts aimed at defining the cellular and molecular elements that comprise renal scars. With regard to the former, it is clear that a profibrotic environment is promoted by activity from a variety of factors with activity driving the production of extracellular matrix (ECM). Of these, TGFβ and other profibrotic cytokines have been widely studied, and these are enhanced by local tissue injury, epithelial cell cycle arrest, cell differentiation status, or hypoxia.1,3