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The kidnapping of mitochondrial function associated with the SARS-CoV-2 infection

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dc.contributor.authorSoria-Castro, Elizabeth
dc.contributor.authorSoto, María Elena
dc.contributor.authorGuarner-Lans, Verónica
dc.contributor.authorRojas, Gustavo
dc.contributor.authorPerezpeña-Diazconti, Mario
dc.contributor.authorCríales-Vera, Sergio A
dc.contributor.authorManzano Pech, Linaloe
dc.contributor.authorPérez-Torres, Israel
dc.date.accessioned2023-01-25T10:07:57Z
dc.date.available2023-01-25T10:07:57Z
dc.date.issued2021
dc.description.abstractInfection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) leads to multiorgan failure associated with a cytokine storm and septic shock. The virus evades the mitochondrial production of interferons through its N protein and, from that moment on, it hijacks the functions of these organelles. The aim of this study was to show how the virus kidnaps the mitochondrial machinery for its benefit and survival, leading to alterations of serum parameters and to nitrosative stress (NSS). In a prospective cohort of 15 postmortem patients who died from COVID-19, six markers of mitochondrial function (COX II, COX IV, MnSOD, nitrotyrosine, Bcl-2 and caspase-9) were analyzed by the immune colloidal gold technique in samples from the lung, heart, and liver. Biometric laboratory results from these patients showed alterations in hemoglobin, platelets, creatinine, urea nitrogen, glucose, C-reactive protein, albumin, D-dimer, ferritin, fibrinogen, Ca2+, K+, lactate and troponin. These changes were associated with alterations in the mitochondrial structure and function. The multi-organ dysfunction present in COVID-19 patients may be caused, in part, by damage to the mitochondria that results in an inflammatory state that contributes to NSS, which activates the sepsis cascade and results in increased mortality in COVID-19 patients.es
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dc.format.extent19es
dc.identifier.citationHistology and Histopathology Vol. 36, nº9 (2021)
dc.identifier.doihttps://doi.org/10.14670/HH-18-354
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/127805
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectSARS-CoV-2es
dc.subjectMitochondriaes
dc.subjectElectron transport chaines
dc.subjectCOVID-19es
dc.subjectNitrosative stresses
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleThe kidnapping of mitochondrial function associated with the SARS-CoV-2 infectiones
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.36, nº9 (2021)