Specific heparanase inhibition reverses glucose-induced mesothelial-to-mesenchymal transition
Author(s) -
Valentina Masola,
Simona Granata,
Gloria Bellin,
Giovanni Gambaro,
Maurizio Onisto,
Carlo Rugiu,
Antonio Lupo,
Gianluigi Zaza
Publication year - 2016
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfw403
Subject(s) - heparanase , epithelial–mesenchymal transition , mesothelial cell , medicine , vascular endothelial growth factor , in vitro , cancer research , cell culture , blot , microbiology and biotechnology , heparan sulfate , biology , pathology , heparin , biochemistry , metastasis , cancer , vegf receptors , genetics , gene
Epithelial-to-mesenchymal transition (EMT) of peritoneal mesothelial cells induced by high glucose (HG) levels is a major biological mechanism leading to myofibroblast accumulation in the omentum of patients on peritoneal dialysis (PD). Heparanase (HPSE), an endoglycosidase that cleaves heparan sulfate chains, is involved in the EMT of several cell lines, and may have a major role in this pro-fibrotic process potentially responsible for the failure of dialysis. Its specific inhibition may therefore plausibly minimize this pathological condition.
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