Muristek
It is now well-established that vascular inflammation contributes to development and progression of atherosclerosis. The potential for vascular inflammation to be a target for treatment began with evidence of benefit from randomized clinical trials of aspirin and statin medications, which have anti-inflammatory among other anti-atherogenic effects. Definitive evidence of the causal treatable nature of vascular inflammation is provided by 3 clinical trials of specific anti-inflammatory agents, including canakinumab and colchicine, which do not have lipid-lowering or antiplatelet effects. Anti-inflammatory therapies for cardiovascular disease that reduced cardiovascular events inhibited the interleukin (IL)-1β, IL-6, and C-reactive protein (CRP) biological pathway. In contrast, methotrexate did not reduce IL-6, CRP, or cardiovascular events. IL-1β is generated from its inactive precursor by the intracellular multimeric NLRP3 inflammasome complex. Activated IL-1β induces and amplifies production of the key inflammatory promoter IL-6, which in turn induces CRP secretion by the liver.
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