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TECHNOLOGICAL ADVANCES IN PERITONEAL DIALYSIS RESEARCH |
Unidad de Biología Molecular,1 Hospital Universitario de la Princesa, Madrid; Departamento de Patología,2 Hospital Universitario de Guadalajara, Guadalajara; Servicio de Nefrología,3 Hospital Universitario La Paz; Servicio de Nefrología,4 Hospital Universitario La Princesa, Madrid, Spain,a
Correspondence to: M. López-Cabrera, Unidad de Biología Molecular, Hospital Universitario de la Princesa, Diego de León, 62, 28006 Madrid, Spain.mlopez.hlpr{at}salud.madrid.org
During peritoneal dialysis (PD), the peritoneum is exposed to
bioincompatible dialysis fluids, which causes progressive fibrosis and
angiogenesis and, ultimately, ultrafiltration failure. In addition, repeated
episodes of peritonitis or hemoperitoneum may accelerate all these processes.
Fibrosis has been classically considered the main cause of peritoneal membrane
functional decline. However, in parallel with fibrosis, the peritoneum also
displays increases in capillary number (angiogenesis) and vasculopathy in
response to PD. Nowadays, there is emerging evidence pointing to peritoneal
microvasculature as the main factor responsible for increased solute transport
and ultrafiltration failure. However, the pathophysiologic mechanism(s)
involved in starting and maintaining peritoneal fibrosis and angiogenesis
remain(s) elusive. Peritoneal stromal fibroblasts have been considered (for
many years) the cell type mainly involved in structural and functional
alterations of the peritoneum; whereas mesothelial cells have been considered
mere victims of peritoneal injury caused by PD. Recently, ex vivo
cultures of effluent-derived mesothelial cells, in conjunction with
immunohistochemical analysis of peritoneal biopsies from PD patients, have
identified mesothelial cells as culprits, at least in part, in peritoneal
membrane deterioration. This review discusses recent findings that suggest new
peritoneal myofibroblastic cells may arise from local conversion of
mesothelial cells by epithelial-to-mesenchymal transition during the repair
responses that take place in PD. The transdifferentiated mesothelial cells may
retain a permanent mesenchymal state, as long as initiating stimuli persist,
and contribute to PD-induced fibrosis and angiogenesis, and hence to membrane
failure. Future therapeutic interventions could be designated in order to
prevent or reverse epithelial-to-mesenchymal transition of mesothelial cells,
or its pernicious effects.
KEY WORDS: Angiogenesis; epithelial-to-mesenchymal transition; fibrosis; mesothelial cells; peritoneal membrane failure; therapeutic intervention; transforming growth factor; vascular endothelial growth factor.
Received 30 May 2005; accepted 19 October 2005.
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  R. Strippoli, I. Benedicto, M. L. Perez Lozano, A. Cerezo, M. Lopez-Cabrera, and M. A. del Pozo Epithelial-to-mesenchymal transition of peritoneal mesothelial cells is regulated by an ERK/NF-{kappa}B/Snail1 pathway Dis. Model. Mech., November 1, 2008; 1(4-5): 264 - 274. [Abstract] [Full Text] [PDF]
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 K. Kaifu, H. Kiyomoto, H. Hitomi, K. Matsubara, T. Hara, K. Moriwaki, G. Ihara, Y. Fujita, N. Sugasawa, D. Nagata, et al. Insulin attenuates apoptosis induced by high glucose via the PI3-kinase/Akt pathway in rat peritoneal mesothelial cells Nephrol. Dial. Transplant., October 30, 2008; (2008) gfn598v1. [Abstract] [Full Text] [PDF]
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