Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease

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 undergo...

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Autores: Gil Fernández, Marta, Navarro García, José Alberto, Val Blasco, Almudena, González Lafuente, Laura, Martínez, José Carlos, Rueda, Angélica, Tamayo, María, Morgado, José Luis, Ruilope Urioste, Luis Miguel, Fernández Velasco, María, Et al.
Formato: artículo
Fecha de publicación:2020
País:España
Recursos:Universidad Europea (UEM)
Repositorio:ABACUS. Repositorio de Producción Científica
Idioma:inglés
OAI Identifier:oai:abacus.universidadeuropea.com:11268/9620
Acesso em linha:http://hdl.handle.net/11268/9620
Access Level:acceso abierto
Palavra-chave:Riñones
Enfermedades
Aparato circulatorio
Enfermedad cardiovascular
Sistema cardiovascular
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spelling Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney DiseaseGil Fernández, MartaNavarro García, José AlbertoVal Blasco, AlmudenaGonzález Lafuente, LauraMartínez, José CarlosRueda, AngélicaTamayo, MaríaMorgado, José LuisRuilope Urioste, Luis MiguelFernández Velasco, MaríaEt al.RiñonesEnfermedadesAparato circulatorioEnfermedad cardiovascularSistema cardiovascularRisk 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.20212021-01-1220202020-01-0120202020-01-01journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/11268/9620reponame:ABACUS. Repositorio de Producción Científicainstname:Universidad Europea (UEM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:abacus.universidadeuropea.com:11268/96202026-06-11T12:41:27Z
dc.title.none.fl_str_mv Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
title Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
spellingShingle Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
Gil Fernández, Marta
Riñones
Enfermedades
Aparato circulatorio
Enfermedad cardiovascular
Sistema cardiovascular
title_short Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
title_full Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
title_fullStr Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
title_full_unstemmed Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
title_sort Genetic Deletion of NOD1 Prevents Cardiac Ca 2+ Mishandling Induced by Experimental Chronic Kidney Disease
dc.creator.none.fl_str_mv Gil Fernández, Marta
Navarro García, José Alberto
Val Blasco, Almudena
González Lafuente, Laura
Martínez, José Carlos
Rueda, Angélica
Tamayo, María
Morgado, José Luis
Ruilope Urioste, Luis Miguel
Fernández Velasco, María
Et al.
author Gil Fernández, Marta
author_facet Gil Fernández, Marta
Navarro García, José Alberto
Val Blasco, Almudena
González Lafuente, Laura
Martínez, José Carlos
Rueda, Angélica
Tamayo, María
Morgado, José Luis
Ruilope Urioste, Luis Miguel
Fernández Velasco, María
Et al.
author_role author
author2 Navarro García, José Alberto
Val Blasco, Almudena
González Lafuente, Laura
Martínez, José Carlos
Rueda, Angélica
Tamayo, María
Morgado, José Luis
Ruilope Urioste, Luis Miguel
Fernández Velasco, María
Et al.
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv
dc.subject.none.fl_str_mv Riñones
Enfermedades
Aparato circulatorio
Enfermedad cardiovascular
Sistema cardiovascular
topic Riñones
Enfermedades
Aparato circulatorio
Enfermedad cardiovascular
Sistema cardiovascular
description 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.
publishDate 2020
dc.date.none.fl_str_mv 2020
2020-01-01
2020
2020-01-01
2021
2021-01-12
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/11268/9620
url http://hdl.handle.net/11268/9620
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:ABACUS. Repositorio de Producción Científica
instname:Universidad Europea (UEM)
instname_str Universidad Europea (UEM)
reponame_str ABACUS. Repositorio de Producción Científica
collection ABACUS. Repositorio de Producción Científica
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.301603

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