The HMGB1-RAGE Inflammatory Pathway: Implications for Brain Injury-Induced Pulmonary Dysfunction

Abstract

Targeting the HMGB1 signaling axis may increase the number of lungs available for transplantation and improve long-term benefits for organ recipient patient outcomes.

Persistent Increase in Microglial RAGE Contributes to Chronic Stress–Induced Priming of Depressive-like Behavior

“…The rapid induction of surface RAGE by 7 d US could result from the persistent elevation of RAGE mRNA expression. RAGE up-regulation and signaling has been implicated in the development and progression of several inflammatory and neurodegenerative diseases (75–85), many of which show high levels of comorbidity with depression. However, this is the first report of long-term, persistent elevated hippocampal RAGE expression in the brain following chronic psychological stress exposure.…”

HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease

“…HMGB1 can bind to both TLR4 and RAGE and has been extensively reviewed by Weber et. al [19]. Their binding abilities depend on the redox states of HMGB1 [19].…”

“…al [19]. Their binding abilities depend on the redox states of HMGB1 [19]. The reduced form contains a thiol group at all three cysteine residues with a serum half-life of 17 min.…”

Ethanol directly induced HMGB1 release through NOX2/NLRP1 inflammasome in neuronal cells

“…Moreover, studies have shown that cognitive deficit is 28 associated with increased neuroinflammation (oxidative-nitro-29 sative stress, TNF-a, IL-1b, and TGF-b1) in both cerebral cortex and 30 hippocampus of ethanol-exposed rats (Tiwari and Chopra, 2012). 31 As cell types of inflammation responding to injury in the brain, it 32 has been long thought that microglial cells are the major CNS (Nadatani et al, 2013;Weber et al, 2015). It has been suggested 57 that brain HMGB1 is highly expressed in neurons and is released 58 from neurons .…”