NAMPTSIRT1 Attenuate Ang II-Induced Vascular Remodeling and Vulnerability to Hypertension by Inhibiting the ROSMAPK Pathway
المؤلفون المشاركون
Zhou, Lei
Zhang, Sheng
Bolor-Erdene, Enkhbat
Wang, Lingwei
Tian, Ding
Mei, Yunqing
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-21، 21ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-12-31
دولة النشر
مصر
عدد الصفحات
21
التخصصات الرئيسية
الملخص EN
Hypertension is characterized by endothelial dysfunction, vascular remodeling, and rearrangement of the extracellular matrix.
Besides, the pathogenesis of hypertension is closely related to excess generation of reactive oxygen species (ROS).
Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent protein deacetylase activity and cleave NAD during the deacetylation cycle.
Recently, NAMPT has been shown to play a crucial role in various diseases associated with oxidative stress.
However, the function and regulation of NAMPT in hypertension have not been extensively explored.
In the present study, we identified NAMPT as a crucial regulator of hypertension, because NAMPT expression was significantly downregulated in both patients with hypertension and experimental animals.
NAMPT knockout (NAMPT+/-) mice exhibited a significantly higher blood pressure and ROS levels after stimulation with angiotensin II (Ang II) than wild-type mice, and the administration of recombinant human NAMPT (rhNAMPT) reversed this effect.
In vivo, overexpression of NAMPT protected against angiotensin II- (Ang II-) induced hypertension by inhibiting ROS production via sirtuin 1 in mouse aortic endothelial cells (MAECs) and mouse aortic vascular smooth muscle cells (MOVAs).
In turn, NAMPT alleviated the ROS-induced mitogen-activated protein kinase (MAPK) pathway.
In conclusion, NAMPT might be a novel biomarker and a therapeutic target in hypertension.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zhou, Lei& Zhang, Sheng& Bolor-Erdene, Enkhbat& Wang, Lingwei& Tian, Ding& Mei, Yunqing. 2020. NAMPTSIRT1 Attenuate Ang II-Induced Vascular Remodeling and Vulnerability to Hypertension by Inhibiting the ROSMAPK Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-21.
https://search.emarefa.net/detail/BIM-1203859
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zhou, Lei…[et al.]. NAMPTSIRT1 Attenuate Ang II-Induced Vascular Remodeling and Vulnerability to Hypertension by Inhibiting the ROSMAPK Pathway. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-21.
https://search.emarefa.net/detail/BIM-1203859
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zhou, Lei& Zhang, Sheng& Bolor-Erdene, Enkhbat& Wang, Lingwei& Tian, Ding& Mei, Yunqing. NAMPTSIRT1 Attenuate Ang II-Induced Vascular Remodeling and Vulnerability to Hypertension by Inhibiting the ROSMAPK Pathway. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-21.
https://search.emarefa.net/detail/BIM-1203859
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203859
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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