High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart

By M. Andrassy, H. C. Volz, J. Igwe, B. Funke, S. Eichberger, Z. Kaya, S. Buss, F. Autschbach, S. Pleger, I. Lukić and 9 more. Circulation, 2008

620 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/21c88f0c53978be2259f4b0af2df91479f0dcc5e

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Citations in the corpus

Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures (2010, background): “Hypoxia has been shown in several scenarios to cause HMGB1 relocation, synthesis or bot”
HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection (2011, background): “In agreement with this mechanism, systemically administered rHMGB1 significantly worsened the severity of damage (103).”
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “improved cardiac remodeling and function after reperfused MI.(15,47) Studies of chimeric mice indicate that RAGE signal-”
HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4 (2012, background): “The HMGB1 dependence of the recruitment of inflammatory cells into damaged tissues was already shown in several animal models, most notably in heart ischemia/reperfusion (Andrassy et al., 2008), in peritonitis (Orlova et al., 2007), and in hepatitis (Sitia et al., 2007, 2011).”
Minocycline: far beyond an antibiotic (2013, background): “In a more recent study, the protective effect of minocycline against myocardial ischaemia and I/R injury was also attributed to inhibition of the expression of high mobility group box 1 (HMGB1), a protein that has been also found to act as an early mediator of inflammation and cell damage during I/R”
Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release (2012, background): “…effects of BoxA in models of hepatitis (Sitia et al., 2007), peritonitis (Orlova et al., 2007), ischemia/reperfusion of the heart and the brain (Andrassy et al., 2008; Muhammad et al., 2008), and other ailments, may be entirely attributable to the reduced recruitment of inflammatory cells in…”
Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities (2018, background): “In support of a pathogenic role for HMGB1, its inhibition following AMI has been reported to be cardioprotective (Andrassy et al., 2008; Hu, Zhang, Jiang, & Hu, 2013).”
Pathophysiology of Myocardial Infarction (2015, neutral): “release of HMGB1 in mediating the postinfarction inflammatory cascade (9, 200).”