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NLRP3 inflammasome is implicated in inflammation-associated diseases such as multiple sclerosis. Liao et al. identified 1,2,4-TTB as a selective NLRP3 inflammasome inhibitor, which inhibited the aggregation of NLRP3 and ameliorated EAE progression and demyelination. This image illustrates the mechanism that 1,2,4-TTB inhibits NLRP3 inflammasome and the progression of EAE. See the article in pages 1769–1779.
Take home Figure. IL-17 promotes the development of heart failure. Upregulation of IL-17 activates NF-κB, which in turn suppresses the expression of CACNA1C encoding the pore-forming subunit of voltage gated Ltype calcium channel Cav1.2 and ATP2A2 encoding SERCA2a. Decreased expression of Cav1.2 and SERCA2a reduced cardiac contractility due to impaired calcium handling and promoted cardiac hypertrophic growth through the activation of calcium related signaling pathway, which eventually led to heart failure. PLN, phospholamban; SERCA2a, sarcoplasmic reticulum Ca2+-ATPase2a; RYR2, ryanodine receptor 2; CAMKII, calcium/calmodulin-dependent kinase II