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Editorial
. 2012 Nov;27(11):3978-81.
doi: 10.1093/ndt/gfs172. Epub 2012 Jul 13.

Twist: a new player in the epithelial-mesenchymal transition of the peritoneal mesothelial cells

Editorial

Twist: a new player in the epithelial-mesenchymal transition of the peritoneal mesothelial cells

Peter J Margetts. Nephrol Dial Transplant. 2012 Nov.

Abstract

Background: The peritoneal membrane is a vital structure for peritoneal dialysis (PD) patients. It has been increasingly recognized that the transition of the peritoneal lining mesothelial cells into a more fibroblastic phenotype is a key step in peritoneal membrane injury.

Methods: Relevant literature was reviewed and summarized.

Results: Epithelial-to-mesenchymal transition (EMT) is a basic cellular process that occurs in a variety of physiologic and pathologic processes. The hallmark of this process is a loss of epithelial markers, and E-cadherin is a prototypical epithelial transmembrane protein. E-cadherin expression is suppressed at many levels and the gene is regulated by a family of transcription factors. Twist is one of the lesser studied E-cadherin regulatory factors, which belongs to a larger family of basic helix-loop-helix DNA-binding proteins. In this issue of Nephrology Dialysis Transplantation, Cuixiang Li reports on in vitro experiments where the expression of Twist led to a decreased expression of E-cadherin and the evidence of EMT. In an in vivo model of dialysate exposure, Li demonstrates that Twist expression is increased in the injured peritoneal tissues.

Conclusions: These important observations are the first to link Twist to mesothelial cell EMT and peritoneal membrane injury. Like most novel observations, this paper leaves many questions unanswered. Twist is only one of several transcription factors involved in EMT and how these factors interact will require further investigations. Furthermore, the question of whether Twist interacts at multiple levels in the EMT process, or simply gives an initial push to the process, is left unanswered. Finally, to bring these early significant findings to the bedside as potential therapies for PD patients will require further innovation.

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