Deng Huidan, Zhu Song, Yang Huiru, Cui Hengmin, Guo Hongrui, Deng Junliang, Ren Zhihua, Geng Yi, Ouyang Ping, Xu Zhiwen, Deng Youtian, Zhu Yanqiu
College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, 611130, China.
Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang, Chengdu, 611130, China.
Biol Trace Elem Res. 2023 Feb;201(2):539-548. doi: 10.1007/s12011-022-03171-0. Epub 2022 Mar 21.
Copper (Cu) is an essential micronutrient for both human and animals. However, excessive intake of copper will cause damage to organs and cells. Inflammation is a biological response that can be induced by various factors such as pathogens, damaged cells, and toxic compounds. Dysregulation of inflammatory responses are closely related to many chronic diseases. Recently, Cu toxicological and inflammatory effects have been investigated in various animal models and cells. In this review, we summarized the known effect of Cu on inflammatory responses and sum up the molecular mechanism of Cu-regulated inflammation. Excessive Cu exposure can modulate a huge number of cytokines in both directions, increase and/or decrease through a variety of molecular and cellular signaling pathways including nuclear factor kappa-B (NF-κB) pathway, mitogen-activated protein kinase (MAPKs) pathway, JAK-STAT (Janus Kinase- signal transducer and activator of transcription) pathway, and NOD-like receptor protein 3 (NLRP3) inflammasome. Underlying the molecular mechanism of Cu-regulated inflammation could help further understanding copper toxicology and copper-associated diseases.
铜（Cu）是人类和动物必需的微量营养素。然而，过量摄入铜会对器官和细胞造成损害。炎症是一种生物学反应，可由病原体、受损细胞和有毒化合物等多种因素诱导。炎症反应失调与许多慢性疾病密切相关。最近，已在各种动物模型和细胞中研究了铜的毒理学和炎症效应。在本综述中，我们总结了铜对炎症反应的已知影响，并归纳了铜调节炎症的分子机制。过量接触铜可通过多种分子和细胞信号通路，包括核因子κB（NF-κB）通路、丝裂原活化蛋白激酶（MAPKs）通路、JAK-STAT（Janus激酶-信号转导和转录激活因子）通路以及NOD样受体蛋白3（NLRP3）炎性小体，双向调节大量细胞因子，使其增加和/或减少。了解铜调节炎症的分子机制有助于进一步理解铜毒理学和与铜相关的疾病。
