Are the Mesothelial-to-Mesenchymal Transition, Sclerotic Peritonitis Syndromes, and Encapsulating Peritoneal Sclerosis Part of the Same Process?

Figure 1

Mechanism for MMT, SPS, and EPS induction as a single process. The PD fluids bioincompatibility induces overproduction of TGF-β that initiates and perpetuates the MMT. MMT includes angiogenesis (VEGF), decreased in fibrinolytic capacity by decrease in tPA, increased in extracellular matrix component production (collagen-1, fibronectin, etc.), and migration mediated by MMPs. MCs lost their gene expression of E-cadherin, cytokeratins, and other and gain the expression of snail, slag, N-cadherin, and so forth. All of these changes become to peritoneal fibrosis and sclerotic peritoneal syndromes (SPS) which are originally reversible. MMT increases in parallel to fibrosis but its role in EPS pathogenesis is unknown. EPS is considered as irreversible process. ICAM, TGF-β, and Ca-125 expression remains stables.