HMGB1 plays a critical role in vascular inflammation and lesion formation via toll-like receptor 9

High Mobility Group Box 1 Promotes Angiogenesis from Bone Marrow-derived Endothelial Progenitor Cells after Myocardial Infarction

“…In addition, extracellular HMGB1 secreted from activated inflammatory cells responds to tissue damage by acting as a cytokine 12) . An increased extracellular HMGB1 level has been reported in the subacute phase after cell injury 25) . Moreover, extracellular HMGB1 binds to receptors for advanced glycation end products (RAGE), toll-like receptors (TLR)-2, TLR-4 and TLR-9 26) .…”

Toll-like Receptors in the Vascular System: Sensing the Dangers Within

“…The contribution of endosomal TLR7 is beginning to emerge as a mediator of vascular remodeling and foam cell accumulation (Karper et al, 2012). Finally, endosomal TLR9 has been observed to propagate inflammation in response to vascular injury (Erridge et al, 2008;Lopez et al, 2012;Hirata et al, 2013), foam cell accumulation, and lesion formation (Niessner et al, 2006;Kim et al, 2009a;Sorrentino et al, 2010;Karper et al, 2012) and in LDL receptor-deficient mice (Ding et al, 2013).…”

Interferon Regulatory Factor Signalings in Cardiometabolic Diseases

“…TLRs are among the most well-known immune factors that are localized to the cell membrane. In the wire-induced vascular injury, HMGB1 functions as one of crucial endogenous activators of TLRs and participates in the progression of neointima formation, 208 whereas during formation of atherosclerotic plaque, oxidized low-density lipoprotein, amyloid-β, and peptidoglycan can trigger TLR signaling and are closely associated with plaque vulnerability. 186,209 The stimulation of TLRs might ultimately induce the activation of IRFs via multistage factors, eg, MyD88, tripartite motif, TRAF, A20, and IKKs, in various cell types, including macrophages, DCs, endothelial cells, and SMCs, that participate in the progression of atherosclerosis.…”