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dc.contributor.authorMira, Rodrigo G.
dc.contributor.authorQuintanilla, Rodrigo A.
dc.contributor.authorCerpa, Waldo
dc.date.accessioned2024-04-10T01:42:40Z
dc.date.available2024-04-10T01:42:40Z
dc.date.issued2023
dc.identifier10.3390/antiox12020403
dc.identifier.issn20763921
dc.identifier.urihttps://hdl.handle.net/20.500.12728/10668
dc.description.abstractTraumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitochondrial dysfunction. However, up until now, there have been no studies evaluating mitochondrial calcium dynamics. Here, we evaluated mitochondrial calcium dynamics in an mTBI model in mice using isolated hippocampal mitochondria for biochemical studies. We observed that 24 h after mTBI, there is a decrease in mitochondrial membrane potential and an increase in basal matrix calcium levels. These findings are accompanied by increased mitochondrial calcium efflux and no changes in mitochondrial calcium uptake. We also observed an increase in NCLX protein levels and calcium retention capacity. Our results suggest that under mTBI, the hippocampal cells respond by incrementing NCLX levels to restore mitochondrial function. © 2023 by the authors.es_ES
dc.description.sponsorshipCenter for Excellence in Science and Technology, (ACE210009, AFB 170005, PFB 12/2007); Fondo Nacional de Desarrollo Científico y Tecnológico, FONDECYT, (1190620); Agencia Nacional de Investigación y Desarrollo, ANIDes_ES
dc.language.isoenes_ES
dc.publisherMDPIes_ES
dc.subjecthippocampuses_ES
dc.subjectmitochondrial calciumes_ES
dc.subjectNCLXes_ES
dc.subjecttraumatic brain injuryes_ES
dc.titleMild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampuses_ES
dc.typeArticlees_ES


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