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The Dysregulation of Inflammatory Pathways Triggered by Copper Exposure

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Abstract

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.

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Funding

This research was supported by the program for Changjiang scholars and the university innovative research team (IRT 0848), and the Shuangzhi project of Sichuan Agricultural University (03572437; 03573050).

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H. Deng: conceptualization, writing—original draft preparation. S Zhu and H Yang: writing—original draft preparation. J. Deng, Z. Ren Y. Geng, P. Ouyang, Z. Xu, Y. Deng, and Y. Zhu: writing—reviewing and editing. H. Cui and H. Guo: conceptualization, supervision, writing—reviewing and editing.

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Correspondence to Hengmin Cui or Hongrui Guo.

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Deng, H., Zhu, S., Yang, H. et al. The Dysregulation of Inflammatory Pathways Triggered by Copper Exposure. Biol Trace Elem Res 201, 539–548 (2023). https://doi.org/10.1007/s12011-022-03171-0

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