کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474284 | 1550421 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Functional brown adipose tissue limits cardiomyocyte injury and adverse remodeling in catecholamine-induced cardiomyopathy
ترجمه فارسی عنوان
بافت عملکردی بافت چربی قهوه، آسیب های قلبی عروقی و بازسازی نامطلوب در کاردیومیوپاتی ناشی از کاتچولامین را کاهش می دهد
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کلمات کلیدی
PWTLVESDLV end-systolic diametercTnILV end-diastolic diameterLVEDdIVSLV mass indexLVMILVEFMYL3BATAWTGTTFABP3DBPSBPH/R - H / RUcp1 - UCP1insulin tolerance test - آزمون تحمل انسولینMyocardial infarct - انفارکتوس میوکاردisoproterenol - ایزوپروترنولITT - اینجاbrown adipose tissue - بافت چربی قهوه ایleft ventricle - بطن چپglucose tolerance test - تست تحمل گلوکزCardioprotection - حفاظت از قلبposterior wall thickness - ضخامت دیواره خلفیInterventricular septal thickness - ضخامت سپتوم بین دهانهdiastolic blood pressure - فشار خون دیاستولیکsystolic blood pressure - فشار خون سیستولیکcardiac troponin I - قلب تروپونین Iheart failure - نارسایی قلبیwild-type - نوع وحشیfatty acid binding protein 3 - پروتئین اتصال دهنده اسید چرب 3uncoupling protein 1 - پروتئین جدا سازی 1LV ejection fraction - کسر خروج LV
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
Brown adipose tissue (BAT) has well recognized thermogenic properties mediated by uncoupling protein 1 (UCP1); more recently, BAT has been demonstrated to modulate cardiovascular risk factors. To investigate whether BAT also affects myocardial injury and remodeling, UCP1-deficient (UCP1â/â) mice, which have dysfunctional BAT, were subjected to catecholamine-induced cardiomyopathy. At baseline, there were no differences in echocardiographic parameters, plasma cardiac troponin I (cTnI) or myocardial fibrosis between wild-type (WT) and UCP1â/â mice. Isoproterenol infusion increased cTnI and myocardial fibrosis and induced left ventricular (LV) hypertrophy in both WT and UCP1â/â mice. UCP1â/â mice also demonstrated exaggerated myocardial injury, fibrosis, and adverse remodeling, as well as decreased survival. Transplantation of WT BAT to UCP1â/â mice prevented the isoproterenol-induced cTnI increase and improved survival, whereas UCP1â/â BAT transplanted to either UCP1â/â or WT mice had no effect on cTnI release. After 3Â days of isoproterenol treatment, phosphorylated AKT and ERK were lower in the LV's of UCP1â/â mice than in those of WT mice. Activation of BAT was also noted in a model of chronic ischemic cardiomyopathy, and was correlated to LV dysfunction. Deficiency in UCP1, and accompanying BAT dysfunction, increases cardiomyocyte injury and adverse LV remodeling, and decreases survival in a mouse model of catecholamine-induced cardiomyopathy. Myocardial injury and decreased survival are rescued by transplantation of functional BAT to UCP1â/â mice, suggesting a systemic cardioprotective role of functional BAT. BAT is also activated in chronic ischemic cardiomyopathy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 84, July 2015, Pages 202-211
Journal: Journal of Molecular and Cellular Cardiology - Volume 84, July 2015, Pages 202-211
نویسندگان
Robrecht Thoonen, Laura Ernande, Juan Cheng, Yasuko Nagasaka, Vincent Yao, Alexandre Miranda-Bezerra, Chan Chen, Wei Chao, Marcello Panagia, David E. Sosnovik, Dheeraj Puppala, Antonis A. Armoundas, Allyson Hindle, Kenneth D. Bloch, Emmanuel S. Buys,