Redox shift is due to Warburg effect and mitochondrial impairment.
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Toxicity of the spike protein of COVID-19 is a redox shift phenomenon: A novel therapeu... - 0 views
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COVID19 COVID-19 cancer inflammation SARS-CoV-2 spike proteins COVID spikeopathy
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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cell division is the most sophisticated way to release entropy
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redox signaling plays an important role in regulating immune function and inflammation, and disruptions in this signaling can lead to excessive cytokine production and immune system activation
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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People at high risk are the elderly, patients suffering from metabolic syndrome such as obesity, or those suffering from chronic diseases such as cancer or inflammation
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COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
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oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
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inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
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persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
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IL-2 is highly up-regulated in Covid-19 patients [37], and IL-2 is known to significantly stimulate the generation of NO in patients
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Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
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vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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viral reactivation in varicella-zoster virus [55] or hepatitis [56], coagulopathy and resulting stroke and myocarditis following both DNA-based vaccines [57] and RNA-based vaccines
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characteristic of the Warburg effect is present in almost every disease and appears to be a central feature in most of the hallmarks of cancer
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inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
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As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
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Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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Cancer, inflammation, Alzheimer's, and Parkinson's diseases share a common peculiarity, the inability of the cell to export entropy outside the body in the harmless form of heat
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
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MeB + can take a pair of electrons (of H atoms) and MeBH can release this pair easily, so that MeB is partially recycled like a catalyst
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MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
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As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
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ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
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Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
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Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism
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NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond - PMC - 0 views
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Pneumonia is a typical symptom of COVID-19 infection, while acute respiratory distress syndrome (ARDS) and multiple organ failure are common in severe COVID-19 patients
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NETs are important for preventing pathogen invasion, their excessive formation can result in a slew of negative consequences, such as autoimmune inflammation and tissue damage
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SARS-CoV-2 infection has also been linked to increased neutrophil-to-lymphocyte ratios, which is associated with disease severity and clinical prognosis
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NETosis is a special form of programmed cell death in neutrophils, which is characterized by the extrusion of DNA, histones, and antimicrobial proteins in a web-like structure known as neutrophil extracellular traps (NETs)
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increased generation of reactive oxygen species (ROS) is a crucial intracellular process that causes NETosis
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In COVID-19, major NET protein cargos of NETs (i.e., NE, MPO, and histones) are significantly elevated.
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SARS-CoV-2 can also infect host cells through noncanonical receptors such as C-type lectin receptors
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Immunopathological manifestations, including cytokine storms and impaired adaptive immunity, are the primary drivers behind COVID-19, with neutrophil infiltration being suggested as a significant cause
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SARS-CoV-2 and its components (e.g., spike proteins and viral RNA) attach to platelets and increase their activation and aggregation in COVID-19, resulting in vascular injury and thrombosis, both of which are linked to NET formation
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NETosis, leading to aberrant immunity such as cytokine storms, autoimmune disorders, and immunosuppression.
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early bacterial coinfections were more prevalent in COVID-19 patients than those infected with other viruses
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NETosis and NETs may also have a role in the development of post COVID-19 syndromes, including lung fibrosis, neurological disorders, tumor growth, and worsening of concomitant disease
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NETs and other by-products of NETosis have been shown to act as direct inflammation amplifiers. Hyperinflammation
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SARS-CoV-2 drives NETosis and NET formation to allow for the release of free DNA and by-products (e.g., elastases and histones). This may trigger surrounding macrophages and endothelial cells to secrete excessive proinflammatory cytokines and chemokines, which, in turn, enhance NET formation and form a positive feedback of cytokine storms in COVID-19
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NET release enables self-antigen exposure and autoantibody production, thereby increasing the autoinflammatory response
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patients with COVID-19 who have higher anti-NET antibodies are more likely to be detected with positive autoantibodies [e.g., antinuclear antibodies (ANA) and anti-neutrophil cytoplasmic antibodies (ANCA)]
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have weakened adaptive immunity as well as a high level of inflammation
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tumor-associated NETosis and NETs promote an immunosuppressive environment in which anti-tumor immunity is compromised
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can enhance this process by interacting with neutrophils through toll-like receptor 4 (TLR4), platelet factor 4 (PF4), and extracellular vesicle-dependent processes
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Following initial onset of COVID-19, an estimated 50% or more of COVID-19 survivors may develop multi-organ problems (e.g., pulmonary dysfunction and neurologic impairment) or have worsening concomitant chronic illness
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NETs in the bronchoalveolar lavage fluid of severe COVID-19 patients cause EMT in lung epithelial cells
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decreased E-cadherin (an epithelial marker) expression
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Patients with tumors have been shown to be more vulnerable to SARS-CoV-2 infection and subsequent development of severe COVID-19
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patients who have recovered from COVID-19 may have an increased risk of developing cancer or of cancer progression and metastasis
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vitamin C has been tested in phase 2 clinical trials aimed at reducing COVID-19-associated mortality by reducing excessive activation of the inflammatory response
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vitamin C is an antioxidant that significantly attenuates PMA-induced NETosis in healthy neutrophils by scavenging ROS
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