Cadmium exposure caused cardiotoxicity in common carps (Cyprinus carpio L.): miR-9-5p, oxidative stress, energetic impairment, mitochondrial division/fusion imbalance, inflammation, and autophagy

文献类型： 外文期刊

第一作者： Liu, Yuhao

作者： Liu, Yuhao;Lin, Xu;Hao, Zhiyu;Yu, Meijin;Teng, Xiaohua;Sun, Wei;Tang, You;Kang, Lu

作者机构：

关键词： Heavy metal; microRNA-9-5p; Energetic impairment; Mitochondrial dynamics; NF-& kappa;B-COX-2 axis; Autophagic injury

期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.7； 五年影响因子：4.7 ）

ISSN： 1050-4648

年卷期： 2023 年 138 卷

页码：

收录情况： SCI

摘要： Cadmium (Cd), a toxic heavy metal pollutant, is a threat to human and eatable fish health. Common carps are widely cultivated and eaten by humans. However, there are no reports about Cd-damaged common carp hearts. Our experiment attempted to investigate the cardiotoxicity of Cd to common carps by establishing a common carp Cd exposure model. Our results showed that Cd injured hearts. Moreover, Cd treatment induced autophagy via miR-9-5p/Sirt1/mTOR/ULK1 pathway. Cd exposure caused oxidant/antioxidant imbalance and oxidative stress; and led to energetic impairment. Energetic impairment partook in oxidative stress-mediated autophagy through AMPK/mTOR/ULK1 pathway. Furthermore, Cd caused mitochondrial division/fusion imbalance and resulted in inflammatory injury via NF-?B-COX-2-PTGEs and NF-?B-COX-2-TNF-a pathways. Oxidative stress mediated mitochondrial division/fusion imbalance, further induced inflammation and autophagy via OPA1/NF-?B-COX-2-TNF-a-Beclin1 and OPA1/NF-?B-COX-2-TNF-a/P62 pathways under Cd treatment. Taken together, miR-9-5p, oxidative stress, energetic impairment, mitochondrial division/fusion imbalance, inflammation, and autophagy participated in the mechanism of Cd-cardiotoxicity to common carps. Our study revealed harmful effect of Cd on hearts, and provided new information for researches of environmental pollutant toxicity.

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