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dc.contributor.author | Aragón-Vela, Jerónimo | |
dc.contributor.author | Casuso, Rafael A | |
dc.contributor.author | Aparisi, Ana Sagrera | |
dc.contributor.author | Plaza-Díaz, Julio | |
dc.contributor.author | Rueda-Robles, Ascensión | |
dc.contributor.author | Hidalgo-Gutiérrez, Agustín | |
dc.contributor.author | López, Luis Carlos | |
dc.contributor.author | Rodríguez-Carrillo, Andrea | |
dc.contributor.author | Enriquez, Jose Antonio | |
dc.contributor.author | Cogliati, Sara | |
dc.contributor.author | Huertas, Jesús R | |
dc.date.accessioned | 2024-07-02T12:36:39Z | |
dc.date.available | 2024-07-02T12:36:39Z | |
dc.date.issued | 2024-04-17 | |
dc.identifier.citation | J Physiol. 2024 Apr 17. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/19909 | |
dc.description.abstract | In eukaryotic cells, aerobic energy is produced by mitochondria through oxygen uptake. However, little is known about the early mitochondrial responses to moderate hypobaric hypoxia (MHH) in highly metabolic active tissues. Here, we describe the mitochondrial responses to acute MHH in the heart and skeletal muscle. Rats were randomly allocated into a normoxia control group (n = 10) and a hypoxia group (n = 30), divided into three groups (0, 6, and 24 h post-MHH). The normoxia situation was recapitulated at the University of Granada, at 662 m above sea level. The MHH situation was performed at the High-Performance Altitude Training Centre of Sierra Nevada located in Granada at 2320 m above sea level. We found a significant increase in mitochondrial supercomplex assembly in the heart as soon as the animals reached 2320 m above sea level and their levels are maintained 24 h post-exposure, but not in skeletal muscle. Furthermore, in skeletal muscle, at 0 and 6 h, there was increased dynamin-related protein 1 (Drp1) expression and a significant reduction in Mitofusin 2. In conclusion, mitochondria from the muscle and heart respond differently to MHH: mitochondrial supercomplexes increase in the heart, whereas, in skeletal muscle, the mitochondrial pro-fission response is trigged. Considering that skeletal muscle was not actively involved in the ascent when the heart was beating faster to compensate for the hypobaric, hypoxic conditions, we speculate that the different responses to MHH are a result of the different energetic requirements of the tissues upon MHH. KEY POINTS: The heart and the skeletal muscle showed different mitochondrial responses to moderate hypobaric hypoxia. Moderate hypobaric hypoxia increases the assembly of the electron transport chain complexes into supercomplexes in the heart. Skeletal muscle shows an early mitochondrial pro-fission response following exposure to moderate hypobaric hypoxia. | es_ES |
dc.description.sponsorship | Julio Plaza-Diaz is supported by a grant awarded to postdoctoral researchers at foreign universities and research centres from the ‘Fundación Ramón Areces’, Madrid, Spain. The present study was supported by grant PID2022-140453OB-I00 financed by MICIU/AEI/10.13039/501100011033 and the FEDER, UE. Sara Cogliati is a recipient of a ‘Ramón y Cajal fellowship 23013-2017’ founded by MCIN/AEI/10.13039/501100011033 and ‘El FSE invierte en tu futuro’. Research in Sara Cogliati’s lab is supported by the Grant PID2020-114054RA-I00 1001100482 founded by MCIN/AEI/10.13039/501100011033. Luis C. López is supported by grant PID2021-126788OB-I00 from the MICIU/AEI/10.13039/501100011033, Spain, and the ERDF/EU. This research was supported by a Marie S. Curie Global Fellowships within the European Union research and innovation framework programme Horizon Europe (2021-2027) (AHG). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Wiley | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Early heart and skeletal muscle mitochondrial response to a moderate hypobaric hypoxia environment. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 38630964 | es_ES |
dc.identifier.doi | 10.1113/JP285516 | es_ES |
dc.contributor.funder | Fundación Ramón Areces | es_ES |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1469-7793 | es_ES |
dc.relation.publisherversion | 10.1113/JP285516 | es_ES |
dc.identifier.journal | The Journal of physiology | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativa | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2022-140453OB-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/MICIU/AEI/10.13039/501100011033 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2020-114054RA-I00/1001100482 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2021-126788OB-I00 | es_ES |