2008
DOI: 10.1093/ndt/gfn495
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Methylglyoxal induces peritoneal thickening by mesenchymal-like mesothelial cells in rats

Abstract: MGO induced peritoneal fibrous thickening with the proliferation of mesenchymal-like mesothelial cells in vivo. These cells may be transdifferentiated from mesothelial cells by EMT via Snail and play an important role in peritoneal fibrous thickening.

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Cited by 60 publications
(78 citation statements)
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“…46,47 Mesothelial cells also express RAGE 48 and AGEs stimulate the production of matrix components by these cells as well as the synthesis of cytokines and growth factors, such as TGF-b and VEGF. 9, [49][50][51][52] AGEs may also induce MMT in vitro and in vivo, 46,50,51 and they can reduce cell proliferation and induce mesothelial cells apoptosis. 53 Here, we demonstrate that RSG-treatment decreases the peritoneal accumulation of AGEs in PD fluidinstilled mice.…”
Section: Discussionmentioning
confidence: 99%
“…46,47 Mesothelial cells also express RAGE 48 and AGEs stimulate the production of matrix components by these cells as well as the synthesis of cytokines and growth factors, such as TGF-b and VEGF. 9, [49][50][51][52] AGEs may also induce MMT in vitro and in vivo, 46,50,51 and they can reduce cell proliferation and induce mesothelial cells apoptosis. 53 Here, we demonstrate that RSG-treatment decreases the peritoneal accumulation of AGEs in PD fluidinstilled mice.…”
Section: Discussionmentioning
confidence: 99%
“…Repeated exposure to peritoneal dialysis solutions containing high concentrations of glucose is considered to play a central role in the development of peritoneal fibrosis in patients undergoing peritoneal dialysis [3–6]. Glucose is degraded to glucose-degradation products including methylglyoxal, glyoxal, formaldehyde, and 3-deoxyglucosone during heat sterilization [14–16], and these products are further transformed to advanced glycation end-products [14,15,17–19]. Both the glucose-degradation products and advanced glycation end-products have been reported to activate transforming growth factor (TGF)-β 1 signaling in the peritoneal membrane, thus promoting peritoneal fibrosis [14,15,17–20].…”
Section: Mechanism Of Peritoneal Fibrosis Developmentmentioning
confidence: 99%
“…Glucose is degraded to glucose-degradation products including methylglyoxal, glyoxal, formaldehyde, and 3-deoxyglucosone during heat sterilization [14–16], and these products are further transformed to advanced glycation end-products [14,15,17–19]. Both the glucose-degradation products and advanced glycation end-products have been reported to activate transforming growth factor (TGF)-β 1 signaling in the peritoneal membrane, thus promoting peritoneal fibrosis [14,15,17–20]. Activated TGF-β 1 promotes the proliferation of fibroblasts from different origins, including mesothelial cells via mesothelial–mesenchymal transition, bone marrow-derived cells, and endothelial cells, in addition to resident fibroblasts [21–24].…”
Section: Mechanism Of Peritoneal Fibrosis Developmentmentioning
confidence: 99%
“…GDPs are generated in PD solutions during heat sterilization and storage, and contribute to the bioincompatibility of conventional PD www.intechopen.com solutions. MMP-2 levels in the peritoneal effluent increased in models of peritoneal injury induced by methylglyoxal (MGO) or formaldehyde, both extremely toxic GDPs [12,13]. In models of peritoneal injury induced by chlorhexidine gluconate and MGO, abdominal cocoons were often formed, while in models induced by talc and formaldehyde, adhesions of the peritoneum were observed [7-9, 11, 12].…”
Section: Production Of Mmp-2 In Animal Models Of Peritoneal Injurymentioning
confidence: 99%