Garg Nisha Jain
Am J Cardiovasc Dis. 2011;1(3):244-54. Epub 2011 Sep 10.
NOD-like receptors (NLRs) constitute a recently identified family of macromolecules that participate in regulation of innate immune responses. To date, 23 members of the NLR family are identified in humans. Diverse NLRs are stimulated by a broad range of pathogen- or danger-associated molecular patterns, and collectively function as intracellular pattern recognition receptors (PRRs). The most studied inflammasomes are NLRP1 and NLRP3 that process inactive pro-caspase-1 to its active form, allowing the cleavage and subsequent activation of pro-IL-1β and pro-IL-18, and initiation of inflammatory responses. Three models, based upon extracellular ATP/K(+) flux, lysosomal release of cathepsin, and reactive oxygen species, have been proposed to be involved in signaling activation of NLRs and downstream events. In this review, I discuss the current state of knowledge related to the roles of NLRs and inflammasomes in the development of cardiovascular diseases.
NOD样受体（NLRs）是最近发现的一类参与调节先天免疫反应的大分子。迄今为止，在人类中已鉴定出23个NLR家族成员。多种NLRs受到广泛的病原体或危险相关分子模式的刺激，并共同作为细胞内模式识别受体（PRRs）发挥作用。研究最多的炎性小体是NLRP1和NLRP3，它们将无活性的前半胱天冬酶-1加工成其活性形式，从而使前白细胞介素-1β和前白细胞介素-18裂解并随后激活，并引发炎症反应。基于细胞外ATP/K(+)通量、组织蛋白酶的溶酶体释放和活性氧，已提出三种模型参与NLRs的信号激活和下游事件。在这篇综述中，我讨论了与NLRs和炎性小体在心血管疾病发展中的作用相关的当前知识状态。
