The hallmark feature of CKD and its progression to end stage is the presence and severity of interstitial fibrosis. 1, 2 This longrecognized 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, TGFb 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

With regard to the latter, although multiple cell types produce ECM, myofibroblasts are considered a primary contributor to ECM production in interstitial fibrosis. 3 Nevertheless, there has been considerable debate regarding the origin of these interstitial cells and whether they derive from proliferation, circulating fibrocytes, or transition from either epithelial or endothelial sources (EMT or EndoMT). Recently, compelling evidence indicates that myofibroblasts may derive from activated pericytes following detachment from the endothelial cells (ECs) for which they provide support. 4 Although specific arguments for each of the potential sources are beyond the scope of this editorial, a comprehensive perspective on progressive fibrosis requires accommodation of theories regarding both the origin and acceleration of renal scarring. Interestingly, a central common feature present in virtually all models leading to interstitial fibrosis is the reduction in peritubular capillary (PTC) density, which is thought to fuel hypoxia and accelerate the rate offibrosis by directly influencing pathways of ECM production. 1 To date, there is very little