Matches in SemOpenAlex for { <https://semopenalex.org/work/W2947029606> ?p ?o ?g. }
- W2947029606 endingPage "647" @default.
- W2947029606 startingPage "635" @default.
- W2947029606 abstract "Tissue-restorative and proangiogenic functions of neutrophils have been uncovered in models of sterile and ischemic injury, as well as in tumors. Neutrophils are important for limiting microbial invasion at sites of skin or mucosal injury, but they also contribute to tissue restoration during wound healing. At the site of injury, neutrophils initiate healing via direct effects on angiogenesis and cell proliferation. The healing capacities of neutrophils are impaired in patients with chronic diseases associated with compromised healing, such as in diabetes. Understanding the contributions of neutrophils to the healing of different types of injuries will help to uncover potential targets that might be therapeutically exploited in disease states where tissue healing can be compromised. Neutrophils promptly accumulate in large numbers at sites of tissue injury. Injuries to the skin or mucosae disrupt barriers against the external environment, and the bactericidal actions of neutrophils are important in preventing microbial invasion. Neutrophils have also been associated with exacerbated inflammation, for example in non-healing wounds or in conditions such as inflammatory bowel disease (IBD). However, additional neutrophil functions important for angiogenesis and tissue restoration have been uncovered in models of sterile and ischemic injury, as well as in tumors. These functions are also relevant in healing skin and mucosal wounds, and can be impaired in conditions associated with non-healing wounds, such as diabetes. Here, we discuss our current understanding of neutrophil contributions to healing, and how the latter can be compromised in disease. Neutrophils promptly accumulate in large numbers at sites of tissue injury. Injuries to the skin or mucosae disrupt barriers against the external environment, and the bactericidal actions of neutrophils are important in preventing microbial invasion. Neutrophils have also been associated with exacerbated inflammation, for example in non-healing wounds or in conditions such as inflammatory bowel disease (IBD). However, additional neutrophil functions important for angiogenesis and tissue restoration have been uncovered in models of sterile and ischemic injury, as well as in tumors. These functions are also relevant in healing skin and mucosal wounds, and can be impaired in conditions associated with non-healing wounds, such as diabetes. Here, we discuss our current understanding of neutrophil contributions to healing, and how the latter can be compromised in disease. protein complexes that bind neighboring epithelial or endothelial cells together and whose cytoplasmic portion is linked to the actin cytoskeleton. polysaccharide-producing bacteria attaching to each other and to a surface. neutrophils can release granules that contain antibacterial agents including MPO, defensins, lysozyme, serine proteases, and lactoferrin. specifically displayed on the surface of apoptotic cells for their selective clearance by macrophages through phagocytosis. the process by which dying cells are cleared by macrophages. a condition in which elevated concentrations of lipids are found in the blood circulation as a result of diet and lifestyle. formed on the surface of wounds during the healing process; granulation tissue comprises connective tissue and blood vessels. a group of transcription factors that respond to locally reduced oxygen concentrations and which mediate the effects of hypoxia. invaginations of the intestinal mucosa covered by different epithelial cells, for example intestinal stem cells that are found at the base of the crypt. tissue damage observed when blood supply returns following a period of ischemia (oxygen deprivation). a cytotoxic enzyme that is abundantly expressed by neutrophils and, upon degranulation, is released into the extracellular space to kill pathogens. vascular smooth muscle cells and pericytes located around blood vessels; mural cells are important for vascular development and stability. first responders to sites of inflammation harboring antitumor activity through the production and release of proinflammatory chemokines and cytokines. neutrophils recruited at later timepoints following injury compared to N1; they are believed to contribute to healing via active phagocytosis. neutrophils can release their DNA into the extracellular space where it forms a network decorated with antibacterial neutrophil-derived proteins to kill bacteria. a key mediator complex of the innate immune system; the inflammasome is activated by danger signals from damaged cells or pathogens. a mural cell that wraps around the microvasculature and is embedded in the basement membrane; it communicates with endothelial cells to stabilize blood vessels. migration of immune cells from tissues into the blood circulation. secretory proteins within the mucus lining of the gastrointestinal mucosa that are believed to contribute to healing the mucosal epithelium. a consequence of myocardial infarction that is believed to reduce ventricular wall strength owing to high concentrations of matrix metalloproteinases." @default.
- W2947029606 created "2019-06-07" @default.
- W2947029606 creator A5005601243 @default.
- W2947029606 creator A5073181252 @default.
- W2947029606 date "2019-07-01" @default.
- W2947029606 modified "2023-10-15" @default.
- W2947029606 title "The Healing Power of Neutrophils" @default.
- W2947029606 cites W1507275598 @default.
- W2947029606 cites W1531471821 @default.
- W2947029606 cites W1749840105 @default.
- W2947029606 cites W1818684172 @default.
- W2947029606 cites W1889143085 @default.
- W2947029606 cites W1913879859 @default.
- W2947029606 cites W1927075449 @default.
- W2947029606 cites W1931315964 @default.
- W2947029606 cites W1969103696 @default.
- W2947029606 cites W1969233019 @default.
- W2947029606 cites W1973431219 @default.
- W2947029606 cites W1983493319 @default.
- W2947029606 cites W1994606929 @default.
- W2947029606 cites W2001356286 @default.
- W2947029606 cites W2002157461 @default.
- W2947029606 cites W2010886407 @default.
- W2947029606 cites W2016445674 @default.
- W2947029606 cites W2017836021 @default.
- W2947029606 cites W2023962283 @default.
- W2947029606 cites W2025065287 @default.
- W2947029606 cites W2028906750 @default.
- W2947029606 cites W2030364983 @default.
- W2947029606 cites W2030620101 @default.
- W2947029606 cites W2031684439 @default.
- W2947029606 cites W2032227357 @default.
- W2947029606 cites W2038254164 @default.
- W2947029606 cites W2038261534 @default.
- W2947029606 cites W2041428471 @default.
- W2947029606 cites W2045186570 @default.
- W2947029606 cites W2045473545 @default.
- W2947029606 cites W2052616119 @default.
- W2947029606 cites W2053391187 @default.
- W2947029606 cites W2059633339 @default.
- W2947029606 cites W2067659428 @default.
- W2947029606 cites W2072805330 @default.
- W2947029606 cites W2085293124 @default.
- W2947029606 cites W2085939434 @default.
- W2947029606 cites W2088830438 @default.
- W2947029606 cites W2098000380 @default.
- W2947029606 cites W2103706790 @default.
- W2947029606 cites W2103950684 @default.
- W2947029606 cites W2110231257 @default.
- W2947029606 cites W2115390024 @default.
- W2947029606 cites W2118654016 @default.
- W2947029606 cites W2128633611 @default.
- W2947029606 cites W2131610923 @default.
- W2947029606 cites W2136082401 @default.
- W2947029606 cites W2136616132 @default.
- W2947029606 cites W2142036444 @default.
- W2947029606 cites W2144451242 @default.
- W2947029606 cites W2150403127 @default.
- W2947029606 cites W2153055549 @default.
- W2947029606 cites W2154785421 @default.
- W2947029606 cites W2156647135 @default.
- W2947029606 cites W2163105501 @default.
- W2947029606 cites W2163229571 @default.
- W2947029606 cites W2166487831 @default.
- W2947029606 cites W2170164215 @default.
- W2947029606 cites W2172836134 @default.
- W2947029606 cites W2224132120 @default.
- W2947029606 cites W2254774777 @default.
- W2947029606 cites W2286929259 @default.
- W2947029606 cites W2306418883 @default.
- W2947029606 cites W2323788043 @default.
- W2947029606 cites W2326472266 @default.
- W2947029606 cites W2376936448 @default.
- W2947029606 cites W2405505865 @default.
- W2947029606 cites W2516952220 @default.
- W2947029606 cites W2518202562 @default.
- W2947029606 cites W2531155603 @default.
- W2947029606 cites W2579236691 @default.
- W2947029606 cites W2605347881 @default.
- W2947029606 cites W2606833037 @default.
- W2947029606 cites W2621934018 @default.
- W2947029606 cites W2623299623 @default.
- W2947029606 cites W2640452423 @default.
- W2947029606 cites W2755895700 @default.
- W2947029606 cites W2756826923 @default.
- W2947029606 cites W2763257724 @default.
- W2947029606 cites W2770491814 @default.
- W2947029606 cites W2773506213 @default.
- W2947029606 cites W2789473628 @default.
- W2947029606 cites W2791792349 @default.
- W2947029606 cites W2799932713 @default.
- W2947029606 cites W2892642834 @default.
- W2947029606 cites W2901254075 @default.
- W2947029606 cites W2903200328 @default.
- W2947029606 cites W2908752885 @default.
- W2947029606 cites W2910117284 @default.
- W2947029606 cites W2922354437 @default.
- W2947029606 cites W2952564192 @default.