Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Department of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
J Cardiovasc Pharmacol. 2019 Oct;74(4):276-284. doi: 10.1097/FJC.0000000000000704.
Metabolic and immune systems are among the most fundamental requirements for survival. Many metabolic and immune response pathways or nutrient- and pathogen-sensing systems are evolutionarily conserved throughout species. As a result, the immune response and metabolic regulation are highly integrated and the proper function of each is dependent on the other. This interaction between metabolic disturbances and the immune system has been most extensively studied in disorders related to obesity such as insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease. Metabolically induced inflammation seems also to play a role in the development and progression of atherosclerosis including its complications such as myocardial infarction (MI) and post-MI remodeling. There are several lines of evidence suggesting that NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a sensor of metabolic stress linking metabolic disturbances to inflammation. Here, we will discuss the role of the NLRP3 inflammasome in the pathogenesis of obesity and diabetes, 2 important risk factors for atherosclerosis and MI. We will also discuss the role of NLRP3 inflammasome in the interaction between metabolic disturbances and myocardial inflammation during MI and during metabolically induced myocardial remodeling.
代谢和免疫系统是生存的最基本要求之一。许多代谢和免疫反应途径或营养和病原体感应系统在物种间是进化保守的。因此，免疫反应和代谢调节高度整合，彼此的正常功能相互依赖。代谢紊乱与免疫系统之间的这种相互作用在与肥胖相关的疾病中得到了最广泛的研究，如胰岛素抵抗、2 型糖尿病和非酒精性脂肪性肝病。代谢诱导的炎症似乎也在动脉粥样硬化的发展和进展中发挥作用，包括其并发症，如心肌梗死（MI）和 MI 后重塑。有几条证据表明，NOD 样受体家族吡啶结构域包含 3（NLRP3）炎性小体是代谢应激的传感器，将代谢紊乱与炎症联系起来。在这里，我们将讨论 NLRP3 炎性小体在肥胖和糖尿病发病机制中的作用，肥胖和糖尿病是动脉粥样硬化和 MI 的 2 个重要危险因素。我们还将讨论 NLRP3 炎性小体在 MI 期间以及代谢诱导的心肌重塑期间代谢紊乱与心肌炎症之间相互作用中的作用。
