عنوان
پدید آورنده
موضوع
رده
کتابخانه
محل استقرار
شماره کتابشناسی ملی
شماره
LA8j3291n3
عنوان و نام پديدآور
عنوان اصلي
Dynasore protects mitochondria and improves cardiac lusitropy in Langendorff perfused mouse heart.
نام عام مواد
[Article]
نام نخستين پديدآور
Gao, Danchen; Zhang, Li; Dhillon, Ranvir; Hong, Ting-Ting; Shaw, Robin M; Zhu, Jianhua
یادداشتهای مربوط به خلاصه یا چکیده
متن يادداشت
Heart failure due to diastolic dysfunction exacts a major economic, morbidity and mortality burden in the United States. Therapeutic agents to improve diastolic dysfunction are limited. It was recently found that Dynamin related protein 1 (Drp1) mediates mitochondrial fission during ischemia/reperfusion (I/R) injury, whereas inhibition of Drp1 decreases myocardial infarct size. We hypothesized that Dynasore, a small noncompetitive dynamin GTPase inhibitor, could have beneficial effects on cardiac physiology during I/R injury.In Langendorff perfused mouse hearts subjected to I/R (30 minutes of global ischemia followed by 1 hour of reperfusion), pretreatment with 1 µM Dynasore prevented I/R induced elevation of left ventricular end diastolic pressure (LVEDP), indicating a significant and specific lusitropic effect. Dynasore also decreased cardiac troponin I efflux during reperfusion and reduced infarct size. In cultured adult mouse cardiomyocytes subjected to oxidative stress, Dynasore increased cardiomyocyte survival and viability identified by trypan blue exclusion assay and reduced cellular Adenosine triphosphate(ATP) depletion. Moreover, in cultured cells, Dynasore pretreatment protected mitochondrial fragmentation induced by oxidative stress.Dynasore protects cardiac lusitropy and limits cell damage through a mechanism that maintains mitochondrial morphology and intracellular ATP in stressed cells. Mitochondrial protection through an agent such as Dynasore can have clinical benefit by positively influencing the energetics of diastolic dysfunction.
مجموعه
تاريخ نشر
2013
عنوان
UCLA
دسترسی و محل الکترونیکی
نام الکترونيکي
مطالعه متن کتاب اطلاعات رکورد کتابشناسی
نوع ماده
[Article]
کد کاربرگه
275578
اطلاعات دسترسی رکورد
سطح دسترسي
a
تكميل شده
Y
