机译:增强的NF-κB活性通过PARP-1-,SP-1-和COX-2依赖性机制损害2型糖尿病的血管功能。
Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, Louisiana,Department of Physiological Sciences, Eastern Virginia School of Medicine, Norfolk, Virginia;
Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, Louisiana;
Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, Louisiana,Department of Physiological Sciences, Eastern Virginia School of Medicine, Norfolk, Virginia;
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas;
Faculty of Science and Technology, Keio University, Kanagawa, Japan;
Center for Cardiovascular Sciences, Albany Medical College, Albany, New York;
Department of Physiological Sciences, Eastern Virginia School of Medicine, Norfolk, Virginia;
Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, Louisiana,Department of Physiological Sciences, Eastern Virginia School of Medicine, Norfolk, Virginia;
机译:增强的P22〜(PHOX)表达通过P38和ERK1 / 2 MAP激酶依赖性机制损害血管函数在2型糖尿病小鼠中
机译:NADPH氧化酶依赖性机制增强的2型糖尿病小鼠的EGF受体酪氨酸激酶活性削弱了血管功能
机译:2型糖尿病和镰状细胞特质中血管功能改变的机制及后果
机译:餐后高糖血症引起的氧化应激可通过增加组织多普勒和波强度来评估2型糖尿病非高血压患者的心肌能量需求,从而损害心脏/血管功能。
机译:控制I型糖尿病肾血管抗性的机制
机译:增强的NF-κB活性通过2型糖尿病的PARP-1–SP-1–和COX-2依赖性机制损害血管功能。
机译:增强的NF-B活性通过2型糖尿病中的PARP-1 - ,SP-1和COX-2依赖性机制损害血管功能