Angina pectoris, associated with coronary artery disease, a cardiovascular disease where the pain is caused by adverse oxygen supply in the myocardium, results in contractility and discomfort in the chest. Inflammasomes, triggered by stimuli due to infection and cellular stress, have been identified to play a vital role in the progression of cardiovascular disorders and, thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicits out an inflammatory response by the emission of pro-inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K⁺ efflux and Ca²⁺ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome is considered to be one of the factors involved in the progression of coronary artery diseases and has an intricate role in the development of angina pectoris.

冠心病与冠心病有关，冠心病是一种心血管疾病，其疼痛由心肌中不利的氧气供应引起，导致胸部的收缩和不适。已确定由感染和细胞应激引起的刺激触发的炎性体在心血管疾病的进展中起着至关重要的作用，因此会引起多种症状，如心绞痛。Nlrp3炎性小体是心绞痛心绞痛发病机理中的关键因素，它需要激活和主要信号传导来引发炎症。Nlrp3炎性体通过产生ROS（活性氧），激活K ⁺外排和Ca ^2+来释放促炎细胞因子，从而引起炎症反应。并通过激活溶酶体去稳定作用，最终导致焦磷酸化，这是程序性的细胞死亡过程。因此，炎性体被认为是参与冠状动脉疾病进展的因素之一，并且在心绞痛的发生中具有复杂的作用。