کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5893181 | 1568241 | 2016 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitochondrial autophagy in cardiomyopathy
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی تکاملی
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چکیده انگلیسی
Cardiac mitochondria produce vast amounts of ATP through oxidative phosphorylation to maintain contractile function. They are also the primary source of reactive oxygen species, which contribute to mitochondrial dysfunction, cardiomyocyte death, and heart failure. To protect against mitochondrial damage, cardiomyocytes develop well-coordinated quality control mechanisms that maintain the overall mitochondrial health through mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial autophagy (mitophagy). Mitophagy removes dysfunctional mitochondria in the heart not only under normal physiological conditions, but also in response to pathological stresses. Accumulating evidence suggests that mitophagy dysregulation can induce cardiomyocyte death and cardiomyopathy. In this review, we discuss what is currently known about mitophagic mechanisms, regulatory pathways, and function in the heart.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Current Opinion in Genetics & Development - Volume 38, June 2016, Pages 8-15
Journal: Current Opinion in Genetics & Development - Volume 38, June 2016, Pages 8-15
نویسندگان
Mingming Tong, Junichi Sadoshima,