کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10751432 | 1050311 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
PDCD5 protects against cardiac remodeling by regulating autophagy and apoptosis
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Cardiac remodeling, including cardiac hypertrophy and fibrosis, is an important pathological process that can lead to heart failure. A previous study demonstrated that autophagy could represent an active adaptive response in cardiomyocytes that affords protection from cardiac remodeling. In the present study, we investigated the role of an autophagy-related gene, PDCD5 (Programmed cell death 5), in cardiac remodeling induced by β-adrenergic stimulation in vivo. We report for the first time that mice systemically overexpressing PDCD5 (PDCD5tg) were protected from cardiac remodeling. In addition, cardiac function was preserved in PDCD5tg mice in response to isoproterenol (ISO) stimulation. Importantly, basal autophagy was significantly higher in PDCD5tg mice than in the wild-type (WT) mice. Moreover, apoptosis was significantly lower in PDCD5tg mice than in WT mice, among the ISO-induced animals. In summary, our findings reveal that PDCD5 overexpression improves cardiac function and inhibits cardiac remodeling induced by ISO via induction of autophagy and inhibition of apoptosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 461, Issue 2, 29 May 2015, Pages 321-328
Journal: Biochemical and Biophysical Research Communications - Volume 461, Issue 2, 29 May 2015, Pages 321-328
نویسندگان
Shu Zhang, Ge Li, Xin Fu, Yanchao Qi, Mengtao Li, Guang Lu, Jia Hu, Nan Wang, Yingyu Chen, Yun Bai, Ming Cui,