دورية أكاديمية
Type 1 Diabetes Impairs Endothelium-Dependent Relaxation Via Increasing Endothelial Cell Glycolysis Through Advanced Glycation End Products, PFKFB3, and Nox1-Mediated Mechanisms.
العنوان: | Type 1 Diabetes Impairs Endothelium-Dependent Relaxation Via Increasing Endothelial Cell Glycolysis Through Advanced Glycation End Products, PFKFB3, and Nox1-Mediated Mechanisms. |
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المؤلفون: | Atawia, Reem T, Batori, Robert K, Jordan, Coleton R, Kennard, Simone, Antonova, Galina, Bruder-Nascimento, Thiago, Mehta, Vinay, Saeed, Muhammad I, Patel, Vijay S, Fukai, Tohru, Ushio-Fukai, Masuko, Huo, Yuqing, Fulton, David J R, Belin de Chantemèle, Eric J |
المصدر: | Hypertension ; ISSN:1524-4563 ; Volume:80 ; Issue:10 |
بيانات النشر: | Atypon |
سنة النشر: | 2023 |
المجموعة: | PubMed Central (PMC) |
مصطلحات موضوعية: | aorta, diabetes mellitus, type 1, endothelial cells, glycolysis, metabolism, vascular diseases, vasodilatation |
الوصف: | Type 1 diabetes (T1D) is a major cause of endothelial dysfunction. Although cellular bioenergetics has been identified as a new regulator of vascular function, whether glycolysis, the primary bioenergetic pathway in endothelial cells (EC), regulates vascular tone and contributes to impaired endothelium-dependent relaxation (EDR) in T1D remains unknown. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
العلاقة: | https://doi.org/10.1161/HYPERTENSIONAHA.123.21341Test; https://pubmed.ncbi.nlm.nih.gov/37729634Test; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10514399Test/ |
DOI: | 10.1161/HYPERTENSIONAHA.123.21341 |
الإتاحة: | https://doi.org/10.1161/HYPERTENSIONAHA.123.21341Test https://pubmed.ncbi.nlm.nih.gov/37729634Test https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10514399Test/ |
رقم الانضمام: | edsbas.38399353 |
قاعدة البيانات: | BASE |
DOI: | 10.1161/HYPERTENSIONAHA.123.21341 |
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