Cellular senescence determines endothelial cell damage induced by uremia |
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| Authors: | Julia Carracedo,Paula Buendí a,Ana Merino,Sagrario Soriano,Elvira Esquivias,Alejandro Martí n-Malo,Pedro Aljama,Rafael Ramí rez |
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| Affiliation: | 1. Reina Sofía University Hospital, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Avda Menéndez Pidal s/n, 14004 Córdoba, Spain;2. Nephrology Unit, Reina Sofía University Hospital, Avda Menéndez Pidal s/n, 14004 Córdoba, Spain;3. RETICs Red Renal (Instituto de Salud Carlos III), Avda. Monforte de Lemos n° 5, 28029 Madrid, Spain;4. Nephrology Laboratory, IDIBELL, C/ Feixa Ilarga s/n, Pavello Govern, Campus Bellvitge, Planta 4°, Hospitalet de Llobregat, 08907 Barcelona, Spain;5. Physiology Department Módulo II — Planta B, University of Alcalá de Henares, Crta. Madrid — Barcelona Km 33,600, 28805 Madrid, Spain |
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| Abstract: | Renal dysfunction is closely associated with endothelial damage leading to cardiovascular disease. However, the extent to which endothelial damage induced by uremia is modulated by aging is poorly known. Aging can render endothelial cells more susceptible to apoptosis through an oxidative stress-dependent pathway. We examined whether senescence-associated to oxidative stress determines the injury induced by the uremia in endothelial cells. |
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| Keywords: | HUVEC, human umbilical vein endothelial cells ROS, reactive oxygen species CVD, cardiovascular disease SIPS, stress-induced premature senescence CKD, chronic kidney disease MDR-D, modification of diet in renal disease ClCr, creatinine clearance PDs, population doublings Vit C, vitamin C PBS, phosphate-buffered saline RECA-I, rat endothelial cell antigen-1 HE, hydroethidine PI, propidium iodide RTL, relative telomere length IOD, integrated optical density |
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