دورية أكاديمية
Perfluoroalkyl sulfonate induces cardiomyocyte apoptosis via endoplasmic reticulum stress activation and autophagy flux inhibition.
| العنوان: | Perfluoroalkyl sulfonate induces cardiomyocyte apoptosis via endoplasmic reticulum stress activation and autophagy flux inhibition. |
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| المؤلفون: | Wang Y; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China., Yin D; Department of Cardiology, Shenzhen Cardiovascular Minimally Invasive Medical Engineering Technology Research and Development Center, Shenzhen People's Hospital, The First Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China., Sun X; Department of Cardiology, Shenzhen Cardiovascular Minimally Invasive Medical Engineering Technology Research and Development Center, Shenzhen People's Hospital, The First Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China., Zhang W; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China., Ma H; Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, No.106 Zhongshan Er Road, Guangzhou, Guangdong, China., Huang J; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China., Yang C; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China. Electronic address: h1094103@connect.hku.hk., Wang J; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China; State Key Laboratory for Quality Esurance and Sustainable Use of Dao-di Herbs, Artemisinin Research Center, and Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China. Electronic address: jgwang@icmm.ac.cn., Geng Q; Department of Geriatrics, Shenzhen Clinical Research Centre for Geriatrics, Shenzhen People's Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, Guangdong, China. Electronic address: gengqsh@163.net. |
| المصدر: | The Science of the total environment [Sci Total Environ] 2024 Jun 20; Vol. 930, pp. 172582. Date of Electronic Publication: 2024 Apr 21. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0330500 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1026 (Electronic) Linking ISSN: 00489697 NLM ISO Abbreviation: Sci Total Environ Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Amsterdam, Elsevier. |
| مواضيع طبية MeSH: | Endoplasmic Reticulum Stress*/drug effects , Myocytes, Cardiac*/drug effects , Apoptosis*/drug effects , Autophagy*/drug effects , Fluorocarbons*/toxicity , Alkanesulfonic Acids*/toxicity, Humans ; Cell Line ; Environmental Pollutants/toxicity |
| مستخلص: | Perfluoroalkyl sulfonate (PFOS) is a commonly used chemical compound that often found in materials such as waterproofing agents, food packaging, and fire retardants. Known for its stability and persistence in the environment, PFOS can enter the human body through various pathways, including water and the food chain, raising concerns about its potential harm to human health. Previous studies have suggested a cardiac toxicity of PFOS, but the specific cellular mechanisms remained unclear. Here, by using AC16 cardiomyocyte as a model to investigate the molecular mechanisms potential the cardiac toxicity of PFOS. Our findings revealed that PFOS exposure reduced cell viability and induces apoptosis in human cardiomyocyte. Proteomic analysis and molecular biological techniques showed that the Endoplasmic Reticulum (ER) stress-related pathways were activated, while the cellular autophagy flux was inhibited in PFOS-exposed cells. Subsequently, we employed strategies such as autophagy activation and ER stress inhibition to alleviate the PFOS-induced apoptosis in AC16 cells. These results collectively suggest that PFOS-induced ER stress activation and autophagy flux inhibition contribute to cardiomyocyte apoptosis, providing new insights into the mechanisms of PFOS-induced cardiomyocyte toxicity. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests to be declared. (Copyright © 2024 Elsevier B.V. All rights reserved.) |
| فهرسة مساهمة: | Keywords: Autophagy; Cardiomyocyte; Cardiotoxicity; ER stress; Perfluoroalkyl sulfonate |
| المشرفين على المادة: | 0 (Fluorocarbons) 0 (Alkanesulfonic Acids) 9H2MAI21CL (perfluorooctane sulfonic acid) 0 (Environmental Pollutants) |
| تواريخ الأحداث: | Date Created: 20240422 Date Completed: 20240514 Latest Revision: 20240514 |
| رمز التحديث: | 20240514 |
| DOI: | 10.1016/j.scitotenv.2024.172582 |
| PMID: | 38649052 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1879-1026 |
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| DOI: | 10.1016/j.scitotenv.2024.172582 |