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Molecular pathways in peritoneal fibrosis.

Abstract：

:Peritoneal dialysis (PD) is a renal replacement therapy for patients with end-stage renal disease that is equivalent to hemodialysis with respect to adequacy, mortality, and other outcome parameters, yet providing superior quality-of-life measures and cost savings. However, long-term usage of the patient's peritoneal membrane as a dialyzer filter is unphysiological and leads to peritoneal fibrosis, which is a major factor of patient morbidity and PD technique failure, resulting in a transfer to hemodialysis or death. Peritoneal fibrosis pathophysiology involves chronic inflammation and the fibrotic process itself. Frequently, inflammation precedes membrane fibrosis development, although a bidirectional relationship of one inducing the other exists. This review aims at highlighting the histopathological definition of peritoneal fibrosis, outlining the interplay of fibrosis, angiogenesis and epithelial-to-mesenchymal transition (EMT), delineating important fibrogenic pathways involving Smad-dependent and Smad-independent transforming growth factor-β (TGF-β) as well as connective tissue growth factor (CTGF) signaling, and summarizing historic and recent studies of inflammatory pathways involving NOD-like receptor protein 3 (NLRP3)/interleukin (IL)-1β, IL-6, IL-17, and other cytokines.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Balzer MS

doi

10.1016/j.cellsig.2020.109778

subject

Has Abstract

pub_date

2020-11-01 00:00:00

pages

109778

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(20)30255-2

journal_volume

75

pub_type

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