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Epithelial to Mesenchymal Transition and Peritoneal Membrane Failure in Peritoneal Dialysis Patients: Pathologic Significance and Potential Therapeutic Interventions

Luiz S. Aroeira^*, Abelardo Aguilera^*, José A. Sánchez-Tomero, M. Auxiliadora Bajo, Gloria del Peso, José A. Jiménez-Heffernan, Rafael Selgas and Manuel López-Cabrera^*

^* Unidad de Biología Molecular and Servicio de Nefrología, Hospital Universitario de la Princesa, and Servicio de Nefrología, Hospital Universitario La Paz, Madrid, and Departamento de Patología, Hospital Universitario de Guadalajara, Guadalajara, Spain

Correspondence: Dr. Manuel López-Cabrera, Unidad de Biología Molecular, Hospital Universitario de la Princesa, C/ Diego de León 62. 28006-Madrid, Spain. Phone: +34-91-5202334; Fax: +34-91-5202374; E-mail: mlopez.hlpr{at}salud.madrid.org

Peritoneal dialysis (PD) is a form of renal replacement and is based on the use of the peritoneum as a semipermeable membrane across which ultrafiltration and diffusion take place. Nevertheless, continuous exposure to bioincompatible PD solutions and episodes of peritonitis or hemoperitoneum cause acute and chronic inflammation and injury to the peritoneal membrane, which progressively undergoes fibrosis and angiogenesis and, ultimately, ultrafiltration failure. The pathophysiologic mechanisms that are involved in peritoneal functional impairment have remained elusive. Resident fibroblasts and infiltrating inflammatory cells have been considered the main entities that are responsible for structural and functional alterations of the peritoneum. Recent findings, however, demonstrated that new fibroblastic cells may arise from local conversion of mesothelial cells (MC) by epithelial-to-mesenchymal transition (EMT) during the inflammatory and repair responses that are induced by PD and pointed to MC as protagonists of peritoneal membrane deterioration. Submesothelial myofibroblasts, which participate in inflammatory responses, extracellular matrix accumulation, and angiogenesis, can originate from activated resident fibroblasts and from MC through EMT. This heterogeneous origin of myofibroblasts reveals new pathogenic mechanisms and offers novel therapeutic possibilities. This article provides a comprehensive review of recent advances on understanding the mechanisms that are implicated in peritoneal structural alterations, which have allowed the identification of the EMT of MC as a potential therapeutic target of membrane failure.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673