Karasawa Tadayoshi, Takahashi Masafumi
Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498 Japan.
Inflamm Regen. 2017 Sep 11;37:18. doi: 10.1186/s41232-017-0050-9. eCollection 2017.
Atherosclerosis is an inflammatory disease, which is accompanied by the deposition of cholesterol-rich lipids and the infiltration of macrophages. Other well-known features of atherosclerotic lesions include the deposition of cholesterol crystals and calcium phosphate crystals; however, their pathophysiological role remains unclear. Recent studies suggest that cholesterol crystals play a pivotal role in activation of NLRP3 inflammasomes, which regulate caspase-1 activation and the subsequent processing of IL-1β, in atherosclerotic lesions. NLRP3 inflammasomes are essential for the initiation of vascular inflammation during the progression of atherosclerosis. Therefore, the regulatory mechanisms of NLRP3 inflammasomes are regarded as potential targets for atherosclerosis treatment. Here, we review the current knowledge regarding the role of NLRP3 inflammasomes in the progression of atherosclerosis and the prospects for therapeutic approaches targeting NLRP3 inflammasomes.
动脉粥样硬化是一种炎症性疾病,伴有富含胆固醇的脂质沉积和巨噬细胞浸润。动脉粥样硬化病变的其他众所周知的特征包括胆固醇晶体和磷酸钙晶体的沉积;然而,它们的病理生理作用仍不清楚。最近的研究表明,胆固醇晶体在动脉粥样硬化病变中NLRP3炎性小体的激活中起关键作用,NLRP3炎性小体调节半胱天冬酶-1的激活以及随后白细胞介素-1β的加工。NLRP3炎性小体在动脉粥样硬化进展过程中血管炎症的起始中至关重要。因此,NLRP3炎性小体的调节机制被视为动脉粥样硬化治疗的潜在靶点。在此,我们综述了关于NLRP3炎性小体在动脉粥样硬化进展中的作用以及靶向NLRP3炎性小体的治疗方法前景的当前知识。