dc.contributor.author | Gil-Fernández, Marta | |
dc.contributor.author | Navarro-García, José Alberto | |
dc.contributor.author | Val-Blasco, Almudena | |
dc.contributor.author | González-Lafuente, Laura | |
dc.contributor.author | Martínez, José Carlos | |
dc.contributor.author | Rueda, Angélica | |
dc.contributor.author | Tamayo, María | |
dc.contributor.author | Morgado, José Luis | |
dc.contributor.author | Zaragoza Sánchez, Carlos | |
dc.contributor.author | Ruilope, Luis Miguel | |
dc.contributor.author | Delgado, Carmen | |
dc.contributor.author | Ruiz Hurtado, Gema | |
dc.contributor.author | Fernández Velasco, María | |
dc.date.accessioned | 2020-11-27T11:47:56Z | |
dc.date.available | 2020-11-27T11:47:56Z | |
dc.date.issued | 2020 | |
dc.identifier.issn | 1422-0067 | spa |
dc.identifier.uri | http://hdl.handle.net/10641/2118 | |
dc.description.abstract | 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. | spa |
dc.language.iso | eng | spa |
dc.publisher | International Journal of Molecular Sciences | spa |
dc.rights | Atribución-NoComercial-SinDerivadas 3.0 España | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/es/ | * |
dc.subject | NOD1 | spa |
dc.subject | Chronic kidney disease | spa |
dc.title | Genetic Deletion of NOD1 Prevents Cardiac Ca2+ Mishandling Induced by Experimental Chronic Kidney Disease. | spa |
dc.type | journal article | spa |
dc.type.hasVersion | AM | spa |
dc.rights.accessRights | open access | spa |
dc.description.extent | 3399 KB | spa |
dc.identifier.doi | 10.3390/ijms21228868 | spa |
dc.relation.publisherversion | https://www.mdpi.com/1422-0067/21/22/8868 | spa |