Reduced Myocardial Ischemia-Reperfusion Injury in Toll-Like Receptor 4-Deficient Mice

By J. Oyama, C. Blais, Xiaoli Liu, Minying Pu, L. Kobzik, R. Kelly, T. Bourcier. Circulation, 2003

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Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities (2018, background): “Following AMI, the nuclear factor, high mobility group box 1 (HMGB1) is released from necrotic cardiac cells, where it has been shown to act on several PRRs including TLR2, TLR4, TLR9 and RAGE to activate NF-kB following AMI (Ding et al., 2013; Park et al., 2004).”
Pathophysiology of Myocardial Infarction (2015, positive): “dependent proinflammatory signaling following myocardial infarction (12,280,335,367).”
Mesenchymal stromal cell-derived exosomes attenuate myocardial ischaemia-reperfusion injury through miR-182-regulated macrophage polarization (2019, positive): “Several studies have shown that the inhibition of TLR4 is beneficial for alleviating inflammatory responses and lessening additional damage to the already injured myocardium.(30,31) Therefore, we established a myocardial I/R model in TLR4-deficiency mice and wild-type (WT) mice.”
Exosomes as Critical Agents of Cardiac Regeneration Triggered by Cell Therapy (2014, background): “…underlying innate immunity plays a major role in the pathology of sterile inflammation, including MI (Arslan et al., 2010; Feng et al., 2008; Oyama et al., 2004; Singh et al., chrome-stained sections of hearts from each of the three groups (B) decreased scar and increased viable mass in…”