Hypoxia, cytokines and stromal recruitment: parallels between pathophysiology of encapsulating peritoneal sclerosis, endometriosis and peritoneal metastasis.

摘要: Peritoneal response to various kinds of injury involves loss peritoneal mesothelial cells (PMC), danger signalling, epithelial-mesenchymal transition and mesothelial-mesenchymal (MMT). Encapsulating sclerosis (EPS), endometriosis (EM) metastasis (PM) are all characterized by hypoxia formation a vascularized connective tissue stroma mediated vascular endothelial growth factor (VEGF). Transforming factor-β1 (TGF-β1) is constitutively expressed the PMC plays major role in maintenance transformed, inflammatory micro-environment PM, but also EPS EM. Persistently high levels TGF-β1 or stimulation cytokines (interleukin-6 (IL-6)) induce MMT, adhesion fibrosis. enhances inducible factor-1α expression, which drives cell growth, extracellular matrix production migration. Disruption glycocalyx exposure basement membrane release low molecular weight hyaluronan, initiates cascade pro-inflammatory mediators, including (TNF-α, IL-1, IL-6, prostaglandins), factors (TGF-α, TGF-β, platelet-derived factor, VEGF, epidermal factor) fibrin/coagulation (thrombin, Tissue plasminogen activator inhibitor [PAI]-1/2). Chronic inflammation cellular transformation damage-associated patterns, pattern recognition receptors, AGE-RAGE, lactate, cytokines, reactive oxygen species, increased glycolysis, metabolomic reprogramming cancer-associated fibroblasts. The pathogenesis EPS, EM PM shows similarities stromal recruitment wound healing.