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Melatonin Ameliorates the Progression of Atherosclerosis via Mitophagy Activation and NLRP3 Inflammasome Inhibition
المؤلفون المشاركون
Ma, Sai
Han, Dong
Chen, Jiangwei
Li, Congye
Fan, Miaomiao
Cao, Feng
Zhang, Ran
Feng, Jing
Wang, Yabin
Li, Xiang
Ren, Jun
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-09-04
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
The NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3) inflammasome-mediated inflammatory responses are critically involved in the progression of atherosclerosis (AS), which is the essential cause for cardiovascular diseases.
Melatonin has anti-inflammatory properties.
However, little is known about the potential effects of melatonin in the pathological process of AS.
Herein, we demonstrate that melatonin suppressed prolonged NLRP3 inflammasome activation in atherosclerotic lesions by reactive oxygen species (ROS) scavenging via mitophagy in macrophages.
The atherosclerotic mouse model was induced with a high-fat diet using ApoE−/− mice.
Melatonin treatment markedly attenuated AS plaque size and vulnerability.
Furthermore, melatonin decreased NLRP3 inflammasome activation and the consequent IL-1β secretion within atherosclerotic lesions.
Despite the unchanged protein expression, the silent information regulator 3 (Sirt3) activity was elevated in the atherosclerotic lesions in melatonin-treated mice.
In ox-LDL-treated macrophages, melatonin attenuated the NLRP3 inflammasome activation and the inflammatory factors secretion, while this protective effect was abolished by either Sirt3 silence or autophagy inhibitor 3-MA.
Mitochondrial ROS (mitoROS), which was a recognized inducer for NLRP3 inflammasome, was attenuated by melatonin through the induction of mitophagy.
Both Sirt3-siRNA and autophagy inhibitor 3-MA partially abolished the beneficial effects of melatonin on mitoROS clearance and NLRP3 inflammasome activation, indicating the crucial role of Sirt3-mediated mitophagy.
Furthermore, we demonstrated that melatonin protected against AS via the Sirt3/FOXO3a/Parkin signaling pathway.
In conclusion, the current study demonstrated that melatonin prevented atherosclerotic progression, at least in part, via inducing mitophagy and attenuating NLRP3 inflammasome activation, which was mediated by the Sirt3/FOXO3a/Parkin signaling pathway.
Collectively, our study provides insight into melatonin as a new target for therapeutic intervention for AS.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Ma, Sai& Chen, Jiangwei& Feng, Jing& Zhang, Ran& Fan, Miaomiao& Han, Dong…[et al.]. 2018. Melatonin Ameliorates the Progression of Atherosclerosis via Mitophagy Activation and NLRP3 Inflammasome Inhibition. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1212368
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Ma, Sai…[et al.]. Melatonin Ameliorates the Progression of Atherosclerosis via Mitophagy Activation and NLRP3 Inflammasome Inhibition. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-12.
https://search.emarefa.net/detail/BIM-1212368
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Ma, Sai& Chen, Jiangwei& Feng, Jing& Zhang, Ran& Fan, Miaomiao& Han, Dong…[et al.]. Melatonin Ameliorates the Progression of Atherosclerosis via Mitophagy Activation and NLRP3 Inflammasome Inhibition. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1212368
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1212368
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر
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