HMGB1 and injury amplification

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HMGB1 and injury amplification

While apoptotic cell death is believed to be mostly non-reactive and hence a component of development and tissue homeostasis, other forms of cell death such as necrosis and necroptosis are considered reactive, resulting in strong inflammatory responses. In contrast to infection, where non-self molecular signatures trigger immune responses, the mechanisms that trigger inflammatory responses to s...

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The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis.

In contrast to microbially triggered inflammation, mechanisms promoting sterile inflammation remain poorly understood. Damage-associated molecular patterns (DAMPs) are considered key inducers of sterile inflammation following cell death, but the relative contribution of specific DAMPs, including high-mobility group box 1 (HMGB1), is ill defined. Due to the postnatal lethality of Hmgb1-knockout ...

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HMGB1 in renal ischemic injury.

Factors that initiate cellular damage and trigger the inflammatory response cascade and renal injury are not completely understood after renal ischemia-reperfusion injury (IRI). High-mobility group box-1 protein (HMGB1) is a damage-associated molecular pattern molecule that binds to chromatin, but upon signaling undergoes nuclear-cytoplasmic translocation and release from cells. Immunohistochem...

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HMGB1 contributes to kidney ischemia reperfusion injury.

High-mobility group box 1 (HMGB1), a nuclear factor released extracellularly as an inflammatory cytokine, is an endogenous ligand for Toll-like receptor 4 (TLR4). TLR4 activation mediates kidney ischemia-reperfusion injury (IRI), but whether HMGB1 contributes to IRI is unknown. Here, treating wild-type mice with neutralizing anti-HMGB1 antibody protected them against kidney IRI, evidenced by lo...

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Systemic inflammation and remote organ injury following trauma require HMGB1.

High-mobility group box 1 (HMGB1) is a 30-kDa DNA-binding protein that displays proinflammatory cytokine-like properties. HMGB1-dependent inflammatory processes have been demonstrated in models of sterile injury, including ischemia-reperfusion injury and hemorrhagic shock. Here, we tested the hypothesis that the systemic inflammatory response and associated remote organ injury that occur after ...

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ژورنال

عنوان ژورنال: Oncotarget

سال: 2015

ISSN: 1949-2553

DOI: 10.18632/oncotarget.5243