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Nephrol Dial Transplant (2004) 19: 285-288
© ERA–EDTA 2004; all rights reserved

Editorial Comments

Cyclosporin A toxicity, and more: vascular endothelial growth factor (VEGF) steps forward

Carlos Caramelo1, Ma. Victoria Alvarez-Arroyo1, Susana Yagüe1, Yusuke Suzuki1, Ma. Angeles Castilla1, Lara Velasco1, F. Roman Gonzalez-Pacheco1 and Alberto Tejedor2

1Laboratorio de Nefrología-Hipertensión, Clínica de la Concepción, Universidad Autónoma and 2Hospital General Gregorio Marañón, Instituto Reina Sofía de Investigación Nefrológica (IRSIN), Madrid, Spain

Correspondence and offprint requests to: C. Caramelo, MD, Laboratorio de Nefrología e Hipertensión, Clínica de la Concepción, Universidad Autónoma, Av Reyes Católicos 2, 28040, Madrid, Spain. Email: ccaramelo@fjd.es

Keywords: calcineurin; cyclosporin A; endothelial cells; toxicity; tubular cells; vascular endothelial growth factor

The first 150 words of the full text of this article appear below.

Toxic effects, which involve some organs with particular intensity, are the main disadvantage in the therapeutic use of cyclosporin A (CsA). Nephrotoxicity, renal vascular damage and hypertension are most relevant among the undesirable effects. Vascular injury has generally been considered a common-ground factor of all types of CsA-induced organ damage [1–3].

Albeit that vascular smooth muscle cells initially appeared to be the main CsA target [2], the finding of multiple endothelial effects [1,3,4–6] indicates that endothelial cell (EC) toxicity is an emerging feature of CsA-induced vascular injury.

Cyclosporin A, endothelium and VEGF

A main issue related to the mechanisms of the effects of CsA is the putative involvement of vascular endothelial growth factor (VEGF) as a relevant cellular response factor. A reasonable possibility is that VEGF has a key role in the cytoprotective mechanisms against CsA-related cell damage and induction of . . . [Full Text of this Article]

Exogenous VEGF, endogenous VEGF

Intracellular mechanisms of endothelial CsA toxicity


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J. C. Mason, R. Steinberg, E. A. Lidington, A. R. Kinderlerer, M. Ohba, and D. O. Haskard
Decay-accelerating Factor Induction on Vascular Endothelium by Vascular Endothelial Growth Factor (VEGF) Is Mediated via a VEGF Receptor-2 (VEGF-R2)- and Protein Kinase C-{alpha}/{epsilon} (PKC{alpha}/{epsilon})-dependent Cytoprotective Signaling Pathway and Is Inhibited by Cyclosporin A
J. Biol. Chem., October 1, 2004; 279(40): 41611 - 41618.
[Abstract] [Full Text] [PDF]