The Role of NLRP3 Inflammasome Activation Pathway of Hepatic Macrophages in Liver Ischemia-Reperfusion Injury.
The Role of NLRP3 Inflammasome Activation Pathway of Hepatic Macrophages in Liver Ischemia-Reperfusion Injury.
复制标题
肝巨噬细胞炎性小体激活通路NLRP3在肝脏缺血再灌注损伤中的作用
DOI:
10.3389/fimmu.2022.905423
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发表时间:
2022
影响因子:
7.3
通讯作者:
Chen, Diyu
中科院分区:
文献类型:
--
作者:
Wu, Tong;Zhang, Cheng;Shao, Tianfeng;Chen, Jianzhong;Chen, Diyu
Ischemia-reperfusion injury (IRI) is considered an inherent component involved in liver transplantation, which induce early organ dysfunction and failure. And the accumulating evidences indicate that the activation of host innate immune system, especially hepatic macrophages, play a pivotal role in the progression of LIRI. Inflammasomes is a kind of intracellular multimolecular complexes that actively participate in the innate immune responses and proinflammatory signaling pathways. Among them, NLRP3 inflammasome is the best characterized and correspond to regulate caspase-1 activation and the secretion of proinflammatory cytokines in response to various pathogen-derived as well as danger-associated signals. Additionally, NLRP3 is highly expressed in hepatic macrophages, and the assembly of NLRP3 inflammasome could lead to LIRI, which makes it a promising therapeutic target. However, detailed mechanisms about NLRP3 inflammasome involving in the hepatic macrophages-related LIRI is rarely summarized. Here, we review the potential role of the NLRP3 inflammasome pathway of hepatic macrophages in LIRI, with highlights on currently available therapeutic options.
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影响因子:
13.5
作者:
Csak, Timea;Ganz, Michal;Pespisa, Justin;Kodys, Karen;Dolganiuc, Angela;Szabo, Gyongyi
通讯作者:
Szabo, Gyongyi
影响因子:
29.7
作者:
Brubaker SW;Bonham KS;Zanoni I;Kagan JC
通讯作者:
Kagan JC
DOI:
10.5500/wjt.v11.i6.187
发表时间:
2021-06-18
期刊:
World journal of transplantation
影响因子:
--
作者:
Kumar R;Anand U;Priyadarshi RN
通讯作者:
Priyadarshi RN
影响因子:
8
作者:
Ferro, R.;Adamska, A.;Falasca, M.
通讯作者:
Falasca, M.
影响因子:
9
作者:
Li, Jichang;Zhao, Jie;Kong, Xiaoni
通讯作者:
Kong, Xiaoni