Cadmium exposure induces endothelial dysfunction via disturbing lipid metabolism in human microvascular endothelial cells
| العنوان: | Cadmium exposure induces endothelial dysfunction via disturbing lipid metabolism in human microvascular endothelial cells |
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| المؤلفون: | Houxiang Hu, Rongchuan Yue, Zhengping Yu, Chao Zhou, Shengzhong Lu, Xi Yu, Mengyu Liu, Zhou Zhou, Hao Liang, Jing Zeng |
| المصدر: | Journal of Applied Toxicology. 41:775-788 |
| بيانات النشر: | Wiley, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | medicine.medical_specialty, Endothelium, 010501 environmental sciences, Toxicology, 01 natural sciences, 03 medical and health sciences, Internal medicine, Lipid droplet, medicine, Animals, Humans, Endothelial dysfunction, Beta oxidation, Triglycerides, 030304 developmental biology, 0105 earth and related environmental sciences, Membrane Potential, Mitochondrial, chemistry.chemical_classification, 0303 health sciences, Reactive oxygen species, Endothelial Cells, Lipid metabolism, Lipid Metabolism, medicine.disease, Mitochondria, medicine.anatomical_structure, Endocrinology, chemistry, Lipogenesis, Environmental Pollutants, Reactive Oxygen Species, Homeostasis, Cadmium |
| الوصف: | Cadmium (Cd) is an occupational and environmental heavy metal pollutant derived from many sources that is linked to endothelial homeostasis. The endothelium is an important site of Cd deposition, while increasing evidence has revealed there is a close relationship between endothelial dysfunction and abnormal lipid metabolism. However, the effects of the alterations in lipid metabolism on endothelial cells (ECs) after Cd exposure still remain unclear. In our study, human microvascular endothelial cells (HMEC-1) were exposed to 40-μM Cd for 6, 12, or 24 h or 10-, 20-, or 40-μM Cd for 24 h, respectively. The Cd exposure accelerated the decomposition of triglyceride (TG) and resulted in the accumulation of free fatty acids (FFAs). These changes stimulated cytotoxicity, impaired fatty acid oxidation (FAO), induced reactive oxygen species (ROS) generation, altered the mitochondrial membrane potential (MMP), and decreased the ATP content, which eventually led to endothelial dysfunction and cell death. In summary, exposure to cadmium caused endothelial dysfunction by disrupting lipid metabolism in HMEC-1. These changes were mainly due to FFA accumulation and FAO inhibition, which further induced ROS generation and mitochondrial dysfunction. Moreover, our results provide novel insight into understanding the alterations of lipid metabolism induced by Cd exposure in ECs. |
| تدمد: | 1099-1263 0260-437X |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::04dddea4cc3b0e4d1b839c4cb625a94aTest https://doi.org/10.1002/jat.4115Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....04dddea4cc3b0e4d1b839c4cb625a94a |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10991263 0260437X |
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