Chen Ting-Ting, Xiao Feng, Li Nan, Shan Shan, Qi Meng, Wang Zi-Ying, Zhang Sheng-Nan, Wei Wei, Sun Wu-Yi
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-Inflammatory and Immune Medicine, Hefei, Anhui Province, 230032, People's Republic of China.
J Inflamm Res. 2021 Apr 20;14:1575-1590. doi: 10.2147/JIR.S304180. eCollection 2021.
Fibrosis is the final stage of the development of chronic inflammation. It is characterized by excessive deposition of the extracellular matrix, leading to tissue structure damage and organ dysfunction, which is a serious threat to human health and life. However, the molecular mechanism of fibrosis is still unclear. Inflammasome is a molecular complex of proteins that has been becoming a key innate sensor for host immunity and is involved in pyroptosis, pathogen infection, metabolic syndrome, cellular stress, and tumor metastasis. Inflammasome signaling and downstream cytokine responses mediated by the inflammasome have been found to play an important role in fibrosis. The inflammasome regulates the secretion of IL-1β and IL-18, which are both critical for the process of fibrosis. Recently, researches on the function of inflammasome have attracted extensive attention, and data derived from these researches have increased our understanding of the effects and regulation of inflammasome during fibrosis. In this review, we emphasize the growing evidence for both indirect and direct effects of inflammasomes in triggering fibrosis as well as potential novel targets for antifibrotic therapies.
纤维化是慢性炎症发展的最后阶段。其特征是细胞外基质过度沉积，导致组织结构破坏和器官功能障碍，这对人类健康和生命构成严重威胁。然而，纤维化的分子机制仍不清楚。炎性小体是一种蛋白质分子复合物，已成为宿主免疫的关键固有传感器，并参与细胞焦亡、病原体感染、代谢综合征、细胞应激和肿瘤转移。已发现炎性小体信号传导以及由炎性小体介导的下游细胞因子反应在纤维化中起重要作用。炎性小体调节IL-1β和IL-18的分泌，这两者对纤维化过程都至关重要。最近，关于炎性小体功能的研究引起了广泛关注，这些研究的数据增加了我们对炎性小体在纤维化过程中的作用和调节的理解。在本综述中，我们强调了炎性小体在引发纤维化方面的间接和直接作用的越来越多的证据，以及抗纤维化治疗的潜在新靶点。
