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Título: | Genetic Deletion of NOD1 Prevents Cardiac Ca2+ Mishandling Induced by Experimental Chronic Kidney Disease |
Autor: | Gil-Fernández, Marta CSIC; Navarro-García, Jose A.; Val-Blasco, Almudena; González-Lafuente, Laura; Martinez, J. C.; Rueda, Angélica; Tamayo, María CSIC ORCID; Morgado, José Luis CSIC; Zaragoza, Carlos; Ruilope, Luis M.; Delgado, Carmen CSIC ORCID ; Ruiz-Hurtado, Gema CSIC ORCID; Fernández-Velasco, María CSIC ORCID | Palabras clave: | NOD1 Chronic kidney disease RIP2 RyR2 Ca2+ handling |
Fecha de publicación: | 2020 | Editor: | Multidisciplinary Digital Publishing Institute | Citación: | International Journal of Molecular Sciences 21(22): 8868 (2020) | Resumen: | Risk of cardiovascular disease (CVD) increases considerably as renal function declines in chronic kidney disease (CKD). Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) has emerged as a novel innate immune receptor involved in both CVD and CKD. Following activation, NOD1 undergoes a conformational change that allows the activation of the receptor-interacting serine/threonine protein kinase 2 (RIP2), promoting an inflammatory response. We evaluated whether the genetic deficiency of Nod1 or Rip2 in mice could prevent cardiac Ca2+ mishandling induced by sixth nephrectomy (Nx), a model of CKD. We examined intracellular Ca2+ dynamics in cardiomyocytes from Wild-type (Wt), Nod1−/− and Rip2−/− sham-operated or nephrectomized mice. Compared with Wt cardiomyocytes, Wt-Nx cells showed an impairment in the properties and kinetics of the intracellular Ca2+ transients, a reduction in both cell shortening and sarcoplasmic reticulum Ca2+ load, together with an increase in diastolic Ca2+ leak. Cardiomyocytes from Nod1−/−-Nx and Rip2−/−-Nx mice showed a significant amelioration in Ca2+ mishandling without modifying the kidney impairment induced by Nx. In conclusion, Nod1 and Rip2 deficiency prevents the intracellular Ca2+ mishandling induced by experimental CKD, unveiling new innate immune targets for the development of innovative therapeutic strategies to reduce cardiac complications in patients with CKD. | Descripción: | © 2020 by the authors. | Versión del editor: | http://dx.doi.org/10.3390/ijms21228868 | URI: | http://hdl.handle.net/10261/234587 | DOI: | 10.3390/ijms21228868 | ISSN: | 1422-0067 |
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