Guanidino Compounds as Cause of Cardiovascular Damage in Chronic Kidney Disease: An in vitro Evaluation

Abstract : Chronic kidney disease is considered a major cause of cardiovascular risk and non-traditional risk factors remain largely unknown. The in vitro toxicity of 10 guanidino compounds (GCs) was evaluated via a standardized approach on different cell systems of relevance in cardiovascular disease. The parameters evaluated were production of reactive oxygen species, expression of surface molecules, cell proliferation, cytotoxicity and calcification. Several GCs had a stimulatory effect on monocytes and granulocytes (SDMA, creatine and guanidinobutyric acid (GBA)). Some GCs (guandine (G), guanidinosuccinic acid (GSA) and SDMA) inhibited endothelial cell proliferation or reduced calcification in osteoblast-like human VSMC (ADMA, GSA and SDMA). Stimulation of osteoclastogenesis could be demonstrated for ADMA, G, guanidinoacetic acid and GBA in a RAW264.7 cell line. No compounds were cytotoxic to AoSMC or endothelial cells, nor influenced their viability. GCs, especially SDMA, likely contribute to cardiovascular complications in uremia, mainly those related to microinflammation and leukocyte activation. Copyright (C) 2010 S. Karger AG, Basel
Liste complète des métadonnées

https://hal.archives-ouvertes.fr/hal-01610436
Contributeur : Laetitia Dou <>
Soumis le : mercredi 4 octobre 2017 - 17:27:09
Dernière modification le : mardi 30 janvier 2018 - 01:30:00

Lien texte intégral

Identifiants

Collections

Citation

Eva Schepers, Griet Glorieux, Laetitia Dou, Claire Cerini, Nathalie Gayrard, et al.. Guanidino Compounds as Cause of Cardiovascular Damage in Chronic Kidney Disease: An in vitro Evaluation. Blood Purification, Karger, 2010, 30 (4), pp.277-287. 〈10.1159/000320765〉. 〈hal-01610436〉

Partager

Métriques

Consultations de la notice

34