دورية أكاديمية

A role of ROS-dependent defects in mitochondrial dynamic and autophagy in carbon black nanoparticle-mediated myocardial cell damage.

التفاصيل البيبلوغرافية
العنوان: A role of ROS-dependent defects in mitochondrial dynamic and autophagy in carbon black nanoparticle-mediated myocardial cell damage.
المؤلفون: Xu Z; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China. Electronic address: 32620211150853@stu.xmu.edu.cn., Li J; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China. Electronic address: leejing@stu.xmu.edu.cn., Su B; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China., Gao H; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China., Ren M; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China., Lin Y; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China. Electronic address: tjlinyi@xmu.edu.cn., Shen H; State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory & State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, 361102, PR China; Department of Obstetrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, 361003, PR China. Electronic address: hqshen@xmu.edu.cn.
المصدر: Free radical biology & medicine [Free Radic Biol Med] 2024 Aug 01; Vol. 220, pp. 249-261. Date of Electronic Publication: 2024 Apr 30.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Country of Publication: United States NLM ID: 8709159 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-4596 (Electronic) Linking ISSN: 08915849 NLM ISO Abbreviation: Free Radic Biol Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Tarrytown, NY : Elsevier Science
Original Publication: New York : Pergamon, c1987-
مواضيع طبية MeSH: Soot*/toxicity , Myocytes, Cardiac*/metabolism , Myocytes, Cardiac*/drug effects , Myocytes, Cardiac*/pathology , Reactive Oxygen Species*/metabolism , Autophagy*/drug effects , Nanoparticles* , Apoptosis*/drug effects , Membrane Potential, Mitochondrial*/drug effects , Mitochondrial Dynamics*/drug effects, Animals ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Inflammasomes/metabolism ; NF-kappa B/metabolism ; NF-kappa B/genetics ; Acetylcysteine/pharmacology ; Male ; Sirolimus/pharmacology ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondria/drug effects ; Oxidative Stress/drug effects
مستخلص: Carbon black nanoparticles (CBNPs) are widely distributed in the environment and are increasingly recognized as a contributor in the development of cardiovascular disease. A variety of cardiac injuries and diseases result from structural and functional damage to cardiomyocytes. This study explored the mechanisms of CBNPs-mediated myocardial toxicity. CBNPs were given to mice through intra-tracheal instillation and it was demonstrated that the particles can be taken up into the cardiac tissue. Exposure to CBNPs induced cardiomyocyte inflammation and apoptosis. In combination with in vitro experiments, we showed that CBNPs increased the ROS and induced mitochondria fragmentation. Functionally, CBNPs-exposed cardiomyocyte exhibited depolarization of the mitochondrial membrane potential, release of cytochrome c, and activation of pro-apoptotic BAX, thereby initiating programmed cell death. On the other hand, CBNPs impaired autophagy, leading to the inadequate removal of dysfunctional mitochondria. The excess accumulation of damaged mitochondria further stimulated NF-κB activation and triggered the NLRP3 inflammasome pathway. Both the antioxidant N-acetylcysteine and the autophagy activator rapamycin were effective to attenuate the damage of CBNPs on cardiomyocytes. Taken together, this study elucidated the potential mechanism underlying CBNPs-induced myocardial injury and provided a scientific reference for the evaluation and prevention of the CBNPs-related heart risk.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: Apoptosis; CBNPs; Cardiomyocyte; Mitochondrial quality control; NF-κB/NLRP3
المشرفين على المادة: 0 (Soot)
0 (Reactive Oxygen Species)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (Inflammasomes)
0 (NF-kappa B)
0 (Nlrp3 protein, mouse)
WYQ7N0BPYC (Acetylcysteine)
W36ZG6FT64 (Sirolimus)
تواريخ الأحداث: Date Created: 20240502 Date Completed: 20240526 Latest Revision: 20240526
رمز التحديث: 20240527
DOI: 10.1016/j.freeradbiomed.2024.04.241
PMID: 38697491
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-4596
DOI:10.1016/j.freeradbiomed.2024.04.241