2026-06-14T03:32:25Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/52492024-09-27T08:50:09Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
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
funder
Italian Association for Cancer Research
funder
Sapienza University of Rome (Italia)
funder
Ministero dell Istruzione, dell Universita e della Ricerca (Italia)
funder
Ministero della Salute (Italia)
2017-10-30T13:32:27Z
2017-10-30T13:32:27Z
2016
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
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.
eng
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
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MolecularMechanismsUnderlyingPeritoneal_2016
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MolecularMechanismsUnderlyingPeritoneal_2016.txt