1. Nat. Rev. Cardiol. doi:10.1038/nrcardio.2016.185
Figure 1 Biological pathways central to the pathogenesis of acute myocardial infarction (AMI)
Figure 1 | Biological pathways central to the pathogenesis of acute myocardial infarction (AMI). Immediately after AMI, a number of local processes are activated, with release of reactive oxygen species (ROS) and cytokines together with accumulation of circulating neutrophils and monocytes resulting in acute myocardial injury. Remote sites are also activated (such as spleen and bone marrow) via signalling pathways that result in further activation of the immune system and injury. Subsequently, a reparative phase ensues, predominantly mediated by monocytes and T lymphocytes resulting in tissue repair, recovery, and scar formation with upregulation of processes involved in angiogenesis and extracellular matrix deposition. CRP, C-reactive protein; CX3CR1, CX3C chemokine receptor 1; DAMPs, damage-associated molecular patterns; HMGB1, high-mobility group protein B1; HSP, heat-shock protein; IFN, interferon; NLR, NOD-like receptor; NLRP3, NACHT, LRR and PYD domains-containing protein 3; SAA, serum amyloid A; TLR, Toll-like receptor; TNF, tumour necrosis factor; VCAM1, vascular cell adhesion protein 1.
Ruparelia, N. et al. (2016) Inflammatory processes in cardiovascular disease: a route to targeted therapies
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