Fig. 1

Proposed new model of fundamental factors determining the variability in timing, extent, and duration of acute inflammatory responses to tissue urate crystal deposits. The schematic depicts multiple, recently described mediators of the phenotype of acute gouty inflammation that are discussed in detail in the text, with many cited in Table 1. In this model, acute gouty inflammation is depicted as a fire surrounding a woodpile that is meant to pictorially represent tissue urate crystal deposits. The most recently discovered mediators of ignition of acute gouty inflammation, amplification of the process, and damping and extinguishing of the response are listed in the schematic, cited in further detail in Table 1, and discussed at length in the text. AMPK AMP-activated protein kinase, CARD8, Caspase recruitment domain-containing protein 8, Clec12a inhibitory C-type lectin receptor 12a, GM-CSF granulocyte macrophage-colony stimulating factor, HDAC histone deacetylase, IFN-1 type I interferon, IL-1ra IL-1 receptor antagonist, MerTK Mer tyrosine kinase receptor for phosphatidylserine, NET neutrophil extracellular trap, PPAR Peroxisome Proliferator-Activated Receptor γ co-activator 1β (PPARGC1B), PMN neutrophil