TY - JOUR
T1 - Transition of mesothelial cell to fibroblast in peritoneal dialysis
T2 - EMT, stem cell or bystander?
AU - Liu, Yu
AU - Dong, Zheng
AU - Liu, Hong
AU - Zhu, Jiefu
AU - Liu, Fuyou
AU - Chen, Guochun
N1 - Publisher Copyright:
© 2015 International Society for Peritoneal Dialysis.
PY - 2015/1/1
Y1 - 2015/1/1
N2 - Long-term peritoneal dialysis (PD) can lead to fibrotic changes in the peritoneum, characterized by loss of mesothelial cells (MCs) and thickening of the submesothelial area with an accumulation of collagen and myofibroblasts. The origin of myofibroblasts is a central question in peritoneal fibrosis that remains unanswered at present. Numerous clinical and experimental studies have suggested that MCs, through epithelial-mesenchymal transition (EMT), contribute to the pool of peritoneal myofibroblasts. However, recent work has placed significant doubts on the paradigm of EMT in organ fibrogenesis (in the kidney particularly), highlighting the need to reconsider the role of EMT in the generation of myofibroblasts in peritoneal fibrosis. In particular, selective cell isolation and lineage-tracing experiments have suggested the existence of progenitor cells in the peritoneum, which are able to switch to fibroblast-like cells when stimulated by the local environment. These findings highlight the plastic nature of MCs and its contribution to peritoneal fibrogenesis. In this review, we summarize the key findings and caveats of EMT in organ fibrogenesis, with a focus on PD-related peritoneal fibrosis, and discuss the potential of peritoneal MCs as a source of myofibroblasts.
AB - Long-term peritoneal dialysis (PD) can lead to fibrotic changes in the peritoneum, characterized by loss of mesothelial cells (MCs) and thickening of the submesothelial area with an accumulation of collagen and myofibroblasts. The origin of myofibroblasts is a central question in peritoneal fibrosis that remains unanswered at present. Numerous clinical and experimental studies have suggested that MCs, through epithelial-mesenchymal transition (EMT), contribute to the pool of peritoneal myofibroblasts. However, recent work has placed significant doubts on the paradigm of EMT in organ fibrogenesis (in the kidney particularly), highlighting the need to reconsider the role of EMT in the generation of myofibroblasts in peritoneal fibrosis. In particular, selective cell isolation and lineage-tracing experiments have suggested the existence of progenitor cells in the peritoneum, which are able to switch to fibroblast-like cells when stimulated by the local environment. These findings highlight the plastic nature of MCs and its contribution to peritoneal fibrogenesis. In this review, we summarize the key findings and caveats of EMT in organ fibrogenesis, with a focus on PD-related peritoneal fibrosis, and discuss the potential of peritoneal MCs as a source of myofibroblasts.
KW - Epithelial-mesenchymal transition
KW - Fibrosis
KW - Mesothelial cell
KW - Peritoneal dialysis
KW - Progenitor cell
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U2 - 10.3747/pdi.2014.00188
DO - 10.3747/pdi.2014.00188
M3 - Review article
C2 - 25700459
AN - SCOPUS:84930888973
SN - 0896-8608
VL - 35
SP - 14
EP - 25
JO - Peritoneal Dialysis International
JF - Peritoneal Dialysis International
IS - 1
ER -