Cellular Mechanisms of Tissue Fibrosis. 3. Novel mechanisms of kidney fibrosis
Year: 2013
Type: review
Abstract: Chronic kidney disease, defined as loss of kidney function for more than three months, is characterized pathologically by glomerulosclerosis, interstitial fibrosis, tubular atrophy, peritubular capillary rarefaction, and inflammation. Recent studies have identified a previously poorly appreciated, yet extensive population of mesenchymal cells, called either pericytes when attached to peritubular capillaries or resident fibroblasts when embedded in matrix, as the progenitors of scar-forming cells known as myofibroblasts. In response to sustained kidney injury, pericytes detach from the vasculature and differentiate into myofibroblasts, a process not only causing fibrosis, but also directly contributing to capillary rarefaction and inflammation. The interrelationship of these three detrimental processes makes myofibroblasts and their pericyte progenitors an attractive target in chronic kidney disease. In this review, we describe current understanding of the mechanisms of pericyte-to-myofibroblast differentiation during chronic kidney disease, draw parallels with disease processes in the glomerulus, and highlight promising new therapeutic strategies that target pericytes or myofibroblasts. In addition, we describe the critical paracrine roles of epithelial, endothelial, and innate immune cells in the fibrogenic process.
Institution: University of Washington
Language: English
Subfield: Nephrology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G2035582507, G2126305166, Kidney pericytes in vascular regeneration after injury, A Tissue Engineered Human Kidney Microphysiological System, The role of Macrophage Delivered WNT Signaling in kidney injury and repair, G3157180015, Kidney Progenitor Cells in Disease, Pericyte-endothelial cross talk in vascular stability after kidney injury, Diabetes Research Center
OpenAlex ID: W2020124228