List out Inflammatory pathways connected with NETosis?
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Inflammatory pathways connected with NETosis include the activation of the NLRP3 inflammasome . Cholesterol accumulation in myeloid cells can activate the NLRP3 inflammasome, leading to increased neutrophil accumulation and NETosis in atherosclerotic plaques . Additionally, the non-canonical inflammasome can also be activated, causing increased susceptibility to LPS-induced mortality . Cytokine-induced ocular inflammation can also trigger NETosis, as seen in an animal model and in patients with proliferative diabetic retinopathy (PDR) . Furthermore, RSV infection can induce NETosis in neutrophils, involving ROS-dependent mechanisms and signaling pathways such as PI3K/AKT, ERK, and p38 MAPK . The identification of these inflammatory pathways connected with NETosis provides insights into the development of organ injury and potential therapeutic targets .
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| Papers (5) | Insight |
|---|---|
106 Citations | The inflammatory pathways connected with NETosis include PI3K/AKT, ERK, p38 MAPK, and necroptosis signaling pathways involving RIPK1, RIPK3, and MLKL. |
| The inflammatory pathways connected with NETosis include IL-6 and IL-8 in Haemolytic Uraemic Syndrome, citrullinated proteins in Rheumatoid Arthritis, and complement pathways in Glomerulonephritides. | |
Open access•Journal Article 21 Citations | The paper does not specifically mention other inflammatory pathways connected with NETosis. |
192 Citations | The NLRP3 inflammasome is connected with NETosis, as mentioned in the abstract. |
8 Citations | The inflammatory pathways connected with NETosis include oxidative stress and autophagy activation. |
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What are the mechanisms by which netosis promotes cancer?5 answersNETosis, the process of neutrophil extracellular trap (NET) formation, has been implicated in promoting cancer through various mechanisms. NETs, composed of DNA, histones, and granular proteins, are released by neutrophils and can regulate tumor growth, promote angiogenesis, and enhance invasiveness. Increased NETosis has been observed in bladder cancer patients, and this may be mediated by impaired degradation of NETs by plasma DNaseI. NETs have also been found to contribute to cancer-associated pathology, including thrombosis, systemic inflammation, and disease relapse. Platelets have been identified as regulators of tumor-induced NETosis, and the platelet-neutrophil interface is an important consideration in designing therapies targeting cancer-associated pathology. Additionally, the predisposition of neutrophils to release NETs in lung cancer patients compared to healthy controls is still unclear, and the impact of G-CSF on NETosis in cancer differs between human and murine neutrophils. Further research is needed to fully understand the mechanisms by which NETosis promotes cancer.
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What are the most abundant proteins inside NETosis formation?5 answersNeutrophil extracellular traps (NETs) are web-like structures of DNA coated with cytotoxic proteins and histones released by activated neutrophils through a process called NETosis. The most abundant proteins inside NETosis formation include histones, which are involved in chromatin decondensation and extrusion of DNA from cells. Additionally, proteins related to immune response are secreted during NETosis, indicating their role in the early events that lead to nuclear and cell membrane rupture and extracellular DNA release. The specific proteins involved in these processes and their exact roles are not fully understood, but further research is being conducted to elucidate the biochemical pathways and mediators of NETosis.
List out Inflammatory pathways connected with NETosis with respect to lung injury?5 answersInflammatory pathways connected with NETosis in lung injury include the involvement of cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. Macrophage extracellular traps (METs) have also been implicated in the inflammatory process and tissue damage in bronchopulmonary dysplasia (BPD). Additionally, the CXCR1/2 signaling pathway has been identified as a therapeutic target in sepsis-induced lung injury. Furthermore, the activation of peptidyl arginine deiminase 4 (PAD4) and subsequent NETosis has been shown to contribute to lung injury in the context of cutaneous chemical burns. Overall, these studies highlight the role of various inflammatory pathways, such as cGAS-STING, METosis, CXCR1/2 signaling, and PAD4 activation, in the development of lung injury associated with NETosis.