Mechanisms of coronary endothelial dysfunction in diabetes

糖尿病冠状动脉内皮功能障碍的机制

• 批准号: 8138788
• 负责人: Ayako Makino
• 金额: $ 10.22万
• 依托单位: UNIVERSITY OF ILLINOIS AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-04-01 至 2012-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8138788
• 关键词: Accounting; Attenuated; Award; Blood Vessels; Blood capillaries; Cardiac; Cardiovascular system; Cell Communication; Cells; Chronic; Complication; Connexin 43; Connexins; Coronary; Coronary artery; Data; Development; Diabetes Mellitus; Diabetic mouse; Down-Regulation; Endothelial Cells; Functional disorder; Gap Junctions; Gene Expression; Genes; Goals; Heart; Heart failure; Hyperglycemia; Hyperlipidemia; Hypertension; Lead; Learning; Link; Maintenance; Mentorship; Molecular; Morbidity - disease rate; Muscle Cells; Pathogenesis; Pathway interactions; Play; Prostaglandins; Regulation; Research Personnel; Research Project Grants; Resistance; Risk; Risk Factors; Role; Testing; Therapeutic; Transgenic Mice; Translational Research; Vascular Diseases; Vascular Endothelium-Dependent Relaxation; Vascular blood supply; Vascular resistance; Work; base; capillary; density; diabetic; diabetic patient; glycosylation; insight; intercellular communication; mortality; mouse model; novel therapeutic intervention; overexpression; peptide O-linked N-acetylglucosamine-beta-N-acetylglucosaminidase; prevent; protein expression; public health relevance; transcription factor