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
Group items matching
in title, tags, annotations or urlThe impact of oncogenic RAS on redox balance and implications for cancer development | ... - 0 views
Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal... - 0 views
50More
NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond - PMC - 0 views
-
SARS-CoV-2 infection has also been linked to increased neutrophil-to-lymphocyte ratios, which is associated with disease severity and clinical prognosis
- ...40 more annotations...
-
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)
-
increased generation of reactive oxygen species (ROS) is a crucial intracellular process that causes NETosis
-
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
-
In COVID-19, major NET protein cargos of NETs (i.e., NE, MPO, and histones) are significantly elevated.
-
SARS-CoV-2 can also infect host cells through noncanonical receptors such as C-type lectin receptors
-
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
-
NETosis, leading to aberrant immunity such as cytokine storms, autoimmune disorders, and immunosuppression.
-
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
-
early bacterial coinfections were more prevalent in COVID-19 patients than those infected with other viruses
-
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
-
NETs and other by-products of NETosis have been shown to act as direct inflammation amplifiers. Hyperinflammation
-
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
-
NET release enables self-antigen exposure and autoantibody production, thereby increasing the autoinflammatory response
-
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)]
-
can enhance this process by interacting with neutrophils through toll-like receptor 4 (TLR4), platelet factor 4 (PF4), and extracellular vesicle-dependent processes
-
have weakened adaptive immunity as well as a high level of inflammation
-
tumor-associated NETosis and NETs promote an immunosuppressive environment in which anti-tumor immunity is compromised
-
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
-
NETs in the bronchoalveolar lavage fluid of severe COVID-19 patients cause EMT in lung epithelial cells
-
decreased E-cadherin (an epithelial marker) expression
-
Patients with tumors have been shown to be more vulnerable to SARS-CoV-2 infection and subsequent development of severe COVID-19
-
patients who have recovered from COVID-19 may have an increased risk of developing cancer or of cancer progression and metastasis
-
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
-
vitamin C is an antioxidant that significantly attenuates PMA-induced NETosis in healthy neutrophils by scavenging ROS
16More
Ascorbic Acid Chemosensitizes Colorectal Cancer Cells and Synergistically Inhibits Tumo... - 0 views
-
pharmacological concentrations of AA were capable of inducing anti-proliferative, cytotoxic and genotoxic effects
- ...12 more annotations...
-
pharmacological concentrations of AA can sensitize cancer cells to chemotherapy, enhancing its antineoplastic effect
-
synergistic effect with conventional chemotherapeutic drugs is a fact already reported, in various types of cancer, by numerous authors, namely in pancreatic (Espey et al., 2011), prostate (Gilloteaux et al., 2014), lung (Lee et al., 2017), breast (Kurbacher et al., 1996; Wu et al., 2017) and ovarian (Ma et al., 2014) cancers.
-
chemosensitizing effect of vitamin C has already been proven by several authors in various types of cancer
-
intravenous pharmacological concentrations, may not only potentiate the effects of conventional chemotherapy, but also improve the quality of life of cancer patients
-
Combined treatment induced a reduction of 11.5% and 43% in cell viability compared with AA or Iri therapies, respectively, emphasizing the synergistic effect
-
cytotoxic effect occurred with treatment with Iri alone, but also this effect was further potentiated by the presence of AA.
-
association of AA with Oxa showed very promising results, considering that a synergistic effect was demonstrated, in almost all conditions
-
AA and Oxa seem to act synergistically by the activation of the intrinsic pathway of apoptosis, translated on the statistically significant increase of the ratio between BAX and BCL-2 proteins, which in turn is associated with a decrease of Δψm
-
Previous results obtained by our group showed that AA mediates reactive oxygen species (ROS) formation capable of irreparably damaging DNA