Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

By Paola Scaffidi, Tom Misteli, M. Bianchi. Nature, 2002

4,107 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/283ca7716b85d57bdea21e5baeba677d6f6b531d

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Citations in the corpus

Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “High mobility group box I (HMGB1) is one of the proinflammatory molecules passively released by necrotic cells [197].”
The IL-1-Like Cytokine IL-33 Is Constitutively Expressed in the Nucleus of Endothelial Cells and Epithelial Cells In Vivo: A Novel ‘Alarmin’? (2008, background): “Two mechanisms have previously been shown to be involved in the release of chromatin-associated cytokine HMGB1, secretion by activated macrophages after hyperacetylation of lysine residues [22] or passive release by necrotic cells during cell damage or tissue injury [19].”
The role of myeloid cells in the promotion of tumour angiogenesis (2008, background): “It might also involve the release of high mobility group 1 ( HMGB1 ) by necrotic cells in sites of chronic tumour hypoxia and/or ischaemi”
Necrotic death as a cell fate. (2006, background): “While it functions to stabilize nucleosome formation and may act as a transcriptional regulator, it also acts as a proinflammatory molecule when released into the extracellular environment during necrosis (Scaffidi et al. 2002).”
Caspase‐1‐dependent pore formation during pyroptosis leads to osmotic lysis of infected host macrophages (2006, background): “…may contribute to the inflammation and tissue destruction observed in vivo (Everest et al ., 2001; Kaufmann et al ., 2001) via caspase1-dependent production of active IL-1 β and IL-18 and release of inflammatory intracellular contents during lysis (Scaffidi et al ., 2002; Shi et al ., 2003).”
HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2 (2006, background): “HMGB1, released passively by injured or necrotic cells, acts as a proinflammatory cytokine and functions as a major stimulus of necrosis-induced inflammation (2).”
The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1 (2009, methodology): “In contrast, IL-33 and HMGB1 were not released extracellularly in the absence of endothelial cell damage (Fig.”
DAMPs, PAMPs and alarmins: all we need to know about danger (2007, background): “When cells die in a nonprogrammed way, HMGB1 is released in the extracellular medium; in contrast, apoptotic cells modify their chromatin so that HMGB1 binds irreversibly and thus is not released [4].”
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “HMGB1: HMGB1, a loosely associated chromatin protein involved in DNA stabilization and gene control,(24) is a potent mediator of inflammation after tissue injury.(25) HMGB1”
Identification of a key pathway required for the sterile inflammatory response triggered by dying cells (2007, background): “Yet the relatively minor nature of their contribution was surprising because Hmgb1, a nuclear protein released from necrotic cells, has been suggested to be a major trigger of inflammation to necrotic cell”
Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “The concept of CXCR4-dependent release of neutrophils from the bone marrow has recently been challenged by an intravital microscopy study showing that CXCR4 inhibition using plerixafor in mice triggers mobilization of neutrophils from the marginated pool of the lung and simultaneously prevents neutr”
Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “DAMPs can be passively released by necrotic hepatocytes due to the disruption of plasma membrane [25,26].”