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- W3205484404 abstract "Recent data show that activation of nociceptive (sensory) nerves turns on localized inflammation within the innervated area in a retrograde manner (antidromically), even in the absence of tissue injury or molecular markers of foreign invaders. This neuroinflammatory process is activated and sustained by the release of neuronal products, such as neuropeptides, with the subsequent amplification via recruitment of immunocompetent cells, including macrophages and lymphocytes. High mobility group box 1 protein (HMGB1) is a highly conserved, well characterized damage-associated molecular pattern molecule expressed by many cells, including nociceptors and is a marker of inflammatory diseases. In this review, we summarize recent evidence showing that neuronal HMGB1 is required for the development of neuroinflammation, as knock out limited to neurons or its neutralization via antibodies ameliorate injury in models of nerve injury and of arthritis. Further, the results of study show that HMGB1 is actively released during neuronal depolarization and thus plays a previously unrecognized key etiologic role in the initiation and amplification of neuroinflammation. Direct targeting of HMGB1 is a promising approach for novel anti-inflammatory therapy." @default.
- W3205484404 created "2021-10-25" @default.
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- W3205484404 date "2021-10-18" @default.
- W3205484404 modified "2023-10-09" @default.
- W3205484404 title "Neurons Are a Primary Driver of Inflammation via Release of HMGB1" @default.
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- W3205484404 doi "https://doi.org/10.3390/cells10102791" @default.
- W3205484404 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8535016" @default.
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