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Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway

Research Square (Research Square) 2022 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 35 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Waseem Ali, Waseem Ali, Jian Sun, Jian Sun, Hui Zou Jian Sun, Hui Zou Hui Zou Waseem Ali, Waseem Ali, Waseem Ali, Yan Chen, Huayi Qu, Huayi Qu, Huayi Qu, Huayi Qu, Huayi Qu, Huayi Qu, Huayi Qu, Huayi Qu, Waseem Ali, Jian Sun, Huayi Qu, Huayi Qu, Waseem Ali, Waseem Ali, Waseem Ali, Waseem Ali, Waseem Ali, Yan Chen, Jian Sun, Jian Sun, Huayi Qu, Hui Zou Waseem Ali, Waseem Ali, Yan Chen, Yan Chen, Huayi Qu, Waseem Ali, Waseem Ali, Hui Zou Tao Wang, Tao Wang, Hui Zou Jianhong Gu, Yan Yuan, Jianhong Gu, Waseem Ali, Yonggang Ma, Yonggang Ma, Jian Sun, Hui Zou Waseem Ali, Jianhong Gu, Jianhong Gu, Yonggang Ma, Hui Zou Yonggang Ma, Zongping Liu, Yan Yuan, Yonggang Ma, Jianhong Gu, Yonggang Ma, Yonggang Ma, Yonggang Ma, Yonggang Ma, Yonggang Ma, Zongping Liu, Yan Yuan, Hui Zou Yan Yuan, Yan Yuan, Yan Yuan, Zongping Liu, Yan Chen, Jianchun Bian, Yonggang Ma, Yonggang Ma, Yan Yuan, Yan Yuan, Jianchun Bian, Yonggang Ma, Yan Yuan, Yonggang Ma, Yonggang Ma, Jianhong Gu, Yonggang Ma, Jianhong Gu, Yonggang Ma, Yan Yuan, Yan Yuan, Jianhong Gu, Zongping Liu, Zongping Liu, Zongping Liu, Yonggang Ma, Jianchun Bian, Jianchun Bian, Hui Zou Yan Yuan, Yonggang Ma, Zongping Liu, Jianhong Gu, Hui Zou Zongping Liu, Zongping Liu, Hui Zou Jianhong Gu, Zongping Liu, Hui Zou Hui Zou Zongping Liu, Zongping Liu, Hui Zou Jianchun Bian, Jianchun Bian, Hui Zou

Summary

Researchers investigated co-exposure to cadmium and polystyrene microplastics in a mouse liver fibrosis model, finding that combined exposure promoted liver fibrosis progression through activation of the hemichannel-ATP-P2X7 purinergic signaling pathway, with microplastics acting as a carrier that enhanced cadmium bioavailability and toxicity.

Polymers

Body Systems

Hepatic Immune

Study Type In vitro

Abstract Background The widespread use of plastic products and the imperfection of plastic recycling systems have led to a continuous increase in microplastics (PS) in the environment. Microplastics have an adsorption effect and can act as carriers for other pollutants in the environment. Cadmium (Cd) is a heavy metal that interacts with microplastics. However, the potential toxicity of co-exposure of cadmium and microplastics to the body is not clear. This study focuses on the effects of co-exposure to cadmium and microplastics on liver fibrosis and its mechanism. Results In this study investigated, Cd+PS exposure increased superoxide anion production and promoted extracellular ATP release compared with exposure to Cd or PS alone. Cd+PS increased inflammatory cell infiltration, activated the P2X7-NLRP3 signaling pathway, and promoted inflammatory factor release. Cd+PS aggravated Cd- or PS-induced liver fibrosis and induced liver inflammation. In AML12/HSC-T6 cell in vitro poisoning model, exposure of AML12 cells to Cd+PS increased the opening of connexin hemichannels and promoted extracellular ATP release. Treatment of HSC-T6 cells with the supernatant of AML12 cells exposed to Cd+PS significantly promoted HSC-T6 cell activation. Treatment of HSC-T6 cells with different concentrations of ATP produced similar results. TAT-Gap19TFA, an inhibitor of connexin hemichannels, significantly inhibited the ATP release and activation of Cd+PS-treated HSC-T6 cells. Finally, the expression of the ATP receptor P2X7 was silenced in HSC-T6 cells, which significantly inhibited their activation. Conclusion Cadmium and microplastics have a synergistic toxic effect on the liver, destroy the microenvironment in the liver, and promote the development of liver fibrosis through the hemichannel-ATP-P2X7 signaling pathway. Our study reveals the impact of co-exposure to cadmium and microplastics on chronic liver diseases, providing a theoretical basis for disease prevention and treatment.

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