2026-06-14T03:36:07Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/52492024-09-27T08:50:09Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Strippoli, Raffaele author Moreno-Vicente, Roberto author Battistelli, Cecilia author Cicchini, Carla author Noce, Valeria author Amicone, Laura author Marchetti, Alessandra author del Pozo, Miguel Angel author Tripodi, Marco author 2016 Peritoneal dialysis is a form of renal replacement alternative to the hemodialysis. During this treatment, the peritoneal membrane acts as a permeable barrier for exchange of solutes and water. Continual exposure to dialysis solutions, as well as episodes of peritonitis and hemoperitoneum, can cause acute/chronic inflammation and injury to the peritoneal membrane, which undergoes progressive fibrosis, angiogenesis, and vasculopathy, eventually leading to discontinuation of the peritoneal dialysis. Among the different events controlling this pathological process, epithelial to mesenchymal transition of mesothelial cells plays a main role in the induction of fibrosis and in subsequent functional deterioration of the peritoneal membrane. Here, the main extracellular inducers and cellular players are described. Moreover, signaling pathways acting during this process are elucidated, with emphasis on signals delivered by TGF-beta family members and by Toll-like/IL-1 beta receptors. The understanding of molecular mechanisms underlying fibrosis of the peritoneal membrane has both a basic and a translational relevance, since it may be useful for setup of therapies aimed at counteracting the deterioration as well as restoring the homeostasis of the peritoneal membrane. Stem Cells Int. 2016; 2016:3543678 10.1155/2016/3543678 1687-9678 1687-966X Stem Cells International 26941801 http://hdl.handle.net/20.500.12105/5249 TO-MESENCHYMAL TRANSITION NEGATIVE FEEDBACK LOOP GLYCATION END-PRODUCTS E-CADHERIN EXPRESSION NF-KAPPA-B MESOTHELIAL CELLS DIALYSIS PATIENTS GROWTH-FACTOR PULMONARY-FIBROSIS IN-VIVO Molecular Mechanisms Underlying Peritoneal EMT and Fibrosis