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- W2886713406 abstract "The mechanisms underlying secondary brain damage following traumatic brain injury (TBI) remain unclear. A great many studies have demonstrated that inflammatory cascades contribute to brain damage through the activation of immune/inflammatory responses, including the increased release of cytokines and chemokines, and the recruitment of leukocytes. The cells and tissues damaged by primary mechanical injury release a number of endogenous factors acting as damage-associated molecular patterns (DAMPs), which initiate and perpetuate noninfectious inflammatory responses through transduction signaling pathways. Toll-like receptors (TLRs) are a transmembrane receptor family that can recognize the specific DAMPs released from damaged cells and recruit a set of adaptors leading to the activation of downstream kinases and nuclear factors which regulate the expression of inflammatory genes. The activation of inflammatory responses mediated by TLR signaling is closely associated with brain tissue damage and neurological dysfunction following TBI. TLRs and their downstream protein kinases may be potential targets for the treatment of TBI. Modulation of TLR-mediated signaling may attenuate brain damage and improve TBI outcome. In this review, we briefly discuss the role of TLR-mediated signaling in TBI and the new treatments targeting TLR signaling. This article is part of the Special Issue entitled Novel Treatments for Traumatic Brain Injury." @default.
- W2886713406 created "2018-08-22" @default.
- W2886713406 creator A5023386934 @default.
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- W2886713406 date "2019-02-01" @default.
- W2886713406 modified "2023-10-16" @default.
- W2886713406 title "Role of Toll-like receptor mediated signaling in traumatic brain injury" @default.
- W2886713406 cites W103258498 @default.
- W2886713406 cites W1128619375 @default.
- W2886713406 cites W1251497040 @default.
- W2886713406 cites W1503384439 @default.
- W2886713406 cites W1503617838 @default.
- W2886713406 cites W1519633296 @default.
- W2886713406 cites W1530403530 @default.
- W2886713406 cites W1578321066 @default.
- W2886713406 cites W1666980118 @default.
- W2886713406 cites W1739269865 @default.
- W2886713406 cites W1783831484 @default.
- W2886713406 cites W1967046222 @default.
- W2886713406 cites W1967338881 @default.
- W2886713406 cites W1967434989 @default.
- W2886713406 cites W1977432663 @default.
- W2886713406 cites W1981046449 @default.
- W2886713406 cites W1983520000 @default.
- W2886713406 cites W1989123508 @default.
- W2886713406 cites W1995586746 @default.
- W2886713406 cites W1999208144 @default.
- W2886713406 cites W2001747259 @default.
- W2886713406 cites W2004266769 @default.
- W2886713406 cites W2005695657 @default.
- W2886713406 cites W2006074529 @default.
- W2886713406 cites W2006086060 @default.
- W2886713406 cites W2009178440 @default.
- W2886713406 cites W2010495142 @default.
- W2886713406 cites W2010915352 @default.
- W2886713406 cites W2012874552 @default.
- W2886713406 cites W2013700204 @default.
- W2886713406 cites W2017676785 @default.
- W2886713406 cites W2018387223 @default.
- W2886713406 cites W2018585106 @default.
- W2886713406 cites W2021634887 @default.
- W2886713406 cites W2028580069 @default.
- W2886713406 cites W2029357279 @default.
- W2886713406 cites W2031335318 @default.
- W2886713406 cites W2034614987 @default.
- W2886713406 cites W2038020431 @default.
- W2886713406 cites W2040854616 @default.
- W2886713406 cites W2042906495 @default.
- W2886713406 cites W2045475619 @default.
- W2886713406 cites W2055793221 @default.
- W2886713406 cites W2055797258 @default.
- W2886713406 cites W2060351820 @default.
- W2886713406 cites W2061812167 @default.
- W2886713406 cites W2062336318 @default.
- W2886713406 cites W2064745340 @default.
- W2886713406 cites W2068374937 @default.
- W2886713406 cites W2069653261 @default.
- W2886713406 cites W2069842601 @default.
- W2886713406 cites W2070131223 @default.
- W2886713406 cites W2070855360 @default.
- W2886713406 cites W2071638430 @default.
- W2886713406 cites W2074385775 @default.
- W2886713406 cites W2077783001 @default.
- W2886713406 cites W2078150553 @default.
- W2886713406 cites W2079738925 @default.
- W2886713406 cites W2082360021 @default.
- W2886713406 cites W2083120074 @default.
- W2886713406 cites W2084603524 @default.
- W2886713406 cites W2091080691 @default.
- W2886713406 cites W2092157690 @default.
- W2886713406 cites W2094715296 @default.
- W2886713406 cites W2101898118 @default.
- W2886713406 cites W2103811767 @default.
- W2886713406 cites W2104414795 @default.
- W2886713406 cites W2108687552 @default.
- W2886713406 cites W2109491705 @default.
- W2886713406 cites W2115185894 @default.
- W2886713406 cites W2116265877 @default.
- W2886713406 cites W2124439764 @default.
- W2886713406 cites W2133160262 @default.
- W2886713406 cites W2137368645 @default.
- W2886713406 cites W2144032514 @default.
- W2886713406 cites W2148917641 @default.
- W2886713406 cites W2155675112 @default.
- W2886713406 cites W2157630213 @default.
- W2886713406 cites W2158591358 @default.
- W2886713406 cites W2159744238 @default.
- W2886713406 cites W2163410184 @default.
- W2886713406 cites W2169855203 @default.
- W2886713406 cites W2177709136 @default.
- W2886713406 cites W2198738464 @default.
- W2886713406 cites W2274185705 @default.
- W2886713406 cites W2277645594 @default.
- W2886713406 cites W2295605120 @default.
- W2886713406 cites W2329777850 @default.