Abstract

Background and Aims: Atherosclerosis is considered as a chronic inflammatory disease and smoking is one of its major risk factors. However, the underlying molecular basis of smoking-induced atherosclerosis remains unclear. Keeping in view the etiological aspects of the disease, novel mechanisms are needed to be identified. It is well established that Nod-like receptor protein (NLRP3) inflammasome regulates Caspase-1-dependent pro-inflammatory cytokine production i.e. interleukin (IL)-1β and IL-18, mediates the cardiovascular inflammatory responses.

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