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The kidnapping of mitochondrial function associated with the SARS-CoV-2 infection.
Soria-Castro, Elizabeth; Soto, María Elena; Guarner-Lans, Verónica; Rojas, Gustavo; Perezpeña-Diazconti, Mario; Críales-Vera, Sergio A; Manzano Pech, Linaloe; Pérez-Torres, Israel.
  • Soria-Castro E; Cardiovascular Biomedicine Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Soto ME; Immunology Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Guarner-Lans V; Physiology Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Rojas G; Intensive Care Unit, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Perezpeña-Diazconti M; Cardiovascular Biomedicine Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Críales-Vera SA; Computed Tomography Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Manzano Pech L; Cardiovascular Biomedicine Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México.
  • Pérez-Torres I; Cardiovascular Biomedicine Department, Instituto Nacional de Cardiología "Ignacio Chávez", Tlalpan, México City, México. pertorisr@yahoo.com.mx.
Histol Histopathol ; 36(9): 947-965, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1513241
ABSTRACT
Infection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) leads to multi-organ 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, Ca²âº, 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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Nitrosative Stress / COVID-19 / Mitochondria Type of study: Cohort study / Observational study / Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Journal: Histol Histopathol Journal subject: Histology / Pathology Year: 2021 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Nitrosative Stress / COVID-19 / Mitochondria Type of study: Cohort study / Observational study / Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Journal: Histol Histopathol Journal subject: Histology / Pathology Year: 2021 Document Type: Article