Involvement of small Ras GTPases and their effectors in chronic renal disease |
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| Authors: | C Martínez-Salgado A B Rodríguez-Peña J M López-Novoa |
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| Institution: | (1) Unidad de Investigación, Hospital Universitario de Salamanca, Salamanca, Spain;(2) Red Cooperativa de Investigación Renal del Instituto Carlos III (RedinRen), Salamanca, Spain;(3) Centro de Investigación del Cáncer CSIC-USAL, Campus Miguel de Unamuno, Salamanca, Spain;(4) Instituto “Reina Sofía” de Investigación Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Avda. Campo Charro s/n, 37007 Salamanca, Spain |
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| Abstract: | The mechanisms involved in the development of renal fibrosis are poorly understood. Small Ras GTPases control cell proliferation,
differentiation, cellular growth and apoptosis, with cell-specific expression in the kidney. Cytokines, high glucose medium
or advanced glycation end-products activate Ras in different renal cells. Increased Ras activation has been found in experimental
tubulointerstitial fibrosis. Transforming growth factor-β1 (TGF-β1) and Ras signalling pathways are close related: TGF-β1
overcomes Ras mitogenic effects, and Ras counteracts TGF-β signalling. However, Ras activation is also an intracellular signal
transduction point for several molecules (e.g. TGF-β1) involved in kidney damage. Ras isoforms play different roles in regulating extracellular matrix synthesis in fibroblasts
and mesangial cells. These data give evidence for a role for Ras in renal fibrosis, but no reviews are available on the role
of p21 Ras in this process. Thus, our goal is to review the role of Ras activation and signalling in renal fibrosis.
Received 7 June 2007; received after revision 17 September 2007; accepted 1 October 2007 |
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| Keywords: | Mesangial cells Ras renal fibroblasts renal fibrosis transforming growth factor-β 1 tubular epithelial cells |
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