Carotid Body-Mediated Chemoreflex Function in Aging and the Role of Receptor-Interacting Protein Kinase

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dc.article.number1164357
dc.contributor.authorDiaz-Jara E.
dc.contributor.authorSchwarz K.G.
dc.contributor.authorRios-Gallardo A.
dc.contributor.authorToledo C.
dc.contributor.authorAlcayaga J.A.
dc.contributor.authorCourt F.A.
dc.contributor.authorDel Rio R.
dc.contributor.otherCEDEUS (Chile)
dc.date.accessioned2025-05-01T10:33:06Z
dc.date.available2025-05-01T10:33:06Z
dc.date.issued2023
dc.description.abstract© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG.Ventilatory impairment during aging has been linked to carotid body (CB) dysfunction. Anatomical/morphological studies evidenced CB degeneration and reductions in the number of CB chemoreceptor cells during aging. The mechanism(s) related to CB degeneration in aging remains elusive. Programmed cell death encompasses both apoptosis and necroptosis. Interestingly, necroptosis can be driven by molecular pathways related to low-grade inflammation, one hallmark of the aging process. Accordingly, we hypothesized that necrotic cell death dependent on receptor-interacting protein kinase-3 (RIPK3) may contribute, at least in part, to impair CB function during aging. Adult (3 months) and aged (24 months) wild type (WT) and RIPK3-/- mice were used to study chemoreflex function. Aging results in significant reductions in both the hypoxic (HVR) and hypercapnic ventilatory responses (HCVR). Adult RIPK3-/- mice showed normal HVR and HCVR compared to adult WT mice. Remarkable, aged RIPK3-/- mice displayed no reductions in HVR nor in HCVR. Indeed, chemoreflex responses obtained in aged RIPK3-/- KO mice were undistinguishable from the ones obtained in adult WT mice. Lastly, we found high prevalence of breathing disorders during aging and this was absent in aged RIPK3-/- mice. Together our results support a role for RIPK3-mediated necroptosis in CB dysfunction during aging.
dc.description.funderNational Agency for Research and Development
dc.description.funderFondecyt
dc.description.funderANID
dc.format.extent11 páginas
dc.fuente.origenScopus
dc.identifier.doi10.1007/978-3-031-32371-3_21
dc.identifier.eisbn9780128194706
dc.identifier.eissn1549-7828
dc.identifier.isbn9783031764011
dc.identifier.issn00652598
dc.identifier.pubmedid40156360
dc.identifier.scieloidS0718-69242020000300109
dc.identifier.scopusidSCOPUS_ID:85163903216
dc.identifier.urihttps://doi.org/10.1007/978-3-031-32371-3_21
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/103952
dc.identifier.wosidWOS:001159473800022
dc.information.autorucFacultad de Ciencias Biológicas; Del Rio Troncoso Rodrigo Andre; 0000-0003-0315-6660; 126608
dc.issue.numero2
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final201
dc.pagina.inicio195
dc.publisherSpringer
dc.relation.ispartofIntersections Interdisciplinary Research on Architecture, Design, City and Territory
dc.revistaAdvances in experimental medicine and biology
dc.rightsacceso restringido
dc.subjectAging
dc.subjectCarotid body
dc.subjectHypoxia
dc.subjectNecroptosis
dc.subjectRIPK3
dc.subject.ddc620
dc.subject.deweyIngenieríaes_ES
dc.subject.ods11 Sustainable cities and communities
dc.subject.odspa11 Ciudades y comunidades sostenibles
dc.titleCarotid Body-Mediated Chemoreflex Function in Aging and the Role of Receptor-Interacting Protein Kinase
dc.typeartículo
dc.volumen1427
sipa.codpersvinculados126608
sipa.indexScopus
sipa.trazabilidadCarga WOS-SCOPUS;01-05-2025
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