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炎症之于机体是一把双刃剑,适度的炎症反应利于机体对抗外界病原微生物的感染,而失调的炎症反应又会使这把利剑挥向机体自身,过度放大或持续存在的炎症反应是导致机体组织损伤和器质性病变的主要原因.事实上,一直以来炎症就被认为与许多慢性疾病的发生发展有着千丝万缕的联系.鉴于此,Science于2005年提出的125个科学问题中就包括“炎症是否是所有慢性疾病发生的重要原因?”.尽管在2型糖尿病、神经退行性疾病、动脉粥样硬化、痛风及肿瘤等多种严重危害人类健康的重大疾病中都检测到有慢性炎症参与的证据,但是长期以来慢性炎症在这些疾病当中发生的细胞和分子机制并不清楚,相关抗炎干预靶点也并未得到确切鉴定.近年,随着对固有免疫模式识别受体和信号转导机制的深入研究,人们发现,包括NLRP3在内的一些固有免疫模式识别受体通过识别上述慢性疾病当中的危险信号,从而启动炎症反应和疾病的发生,提示NLRP3等固有免疫模式识别受体及其信号通路可能成为包括2型糖尿病在内的相关炎性疾病治疗的新靶点.本文将着重介绍近年有关NLRP3炎症小体活化与T2DM的关系,以及靶向NLRP3炎症小体的T2DM治疗研究方面的进展.
Inflammation of the body is a double-edged sword, moderate inflammatory response conducive to the body against the infection of pathogenic microorganisms outside the body, and the dysregulated inflammatory response will make this sword to the body itself, excessive amplification or persistence of inflammation is Leading to body tissue damage and organic diseases, the main reason.In fact, inflammation has long been thought to be inextricably linked with the occurrence and development of many chronic diseases.In view of this, Science in 2005 proposed 125 scientific issues Include “Is inflammation an important cause of any chronic disease?” Although there are a number of major illnesses that endanger human health such as type 2 diabetes, neurodegenerative diseases, atherosclerosis, gout and cancer Evidence of involvement of chronic inflammation has been detected, but the cellular and molecular mechanisms that chronic inflammation has long been implicated in are not clear, and the relevant anti-inflammatory intervention targets have not been identified yet.In recent years, with the identification of innate immunity patterns Receptor and signal transduction mechanisms, it has been found that some innate immune pattern recognition receptors, including NLRP3, Risk signals among sexually transmitted diseases, thereby initiating the inflammatory response and the occurrence of diseases, suggesting that innate immune pattern recognition receptors such as NLRP3 and their signaling pathways may become new targets for the treatment of related inflammatory diseases including type 2 diabetes. This review focuses on the recent advances in the relationship between activation of NLRP3 inflammasome and T2DM, as well as in the study of T2DM targeting NLRP3 inflammasome.