کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10751070 | 1050306 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acetyl-CoA carboxylase 2 suppression rescues human proximal tubular cells from palmitic acid induced lipotoxicity via autophagy
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Acetyl-CoA carboxylase 2 suppression rescues human proximal tubular cells from palmitic acid induced lipotoxicity via autophagy Acetyl-CoA carboxylase 2 suppression rescues human proximal tubular cells from palmitic acid induced lipotoxicity via autophagy](/preview/png/10751070.png)
چکیده انگلیسی
Autophagy is a catabolic process that degrades damaged proteins and organelles in mammalian cells. Although acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the fatty acid metabolism, it keeps unknown whether ACC2 is associated with autophagic activity. The present work was designed to investigate the effects of ACC2 on palmitic acid (PA) induced lipotoxicity in human proximal tubular cells and the putative role of autophagy in this process. Here we show that autophagy was induced by PA in HK-2 cells. Moreover, the PA induced autophagy was regulated both by ACC2 suppression and CPTI inhibitor treatment, which represent an altered fatty acid β-oxidation. And the knockdown of ACC2 reduced PA-induced autophagy and thus protects the cells from PA-induced lipotoxicity with attenuated lipid accumulation and rescued cell viability. Collectively, the present study proposed a novel autophagy-involved mechanism of PA-induced renal lipotoxicity and provided potential therapeutic strategy by modulating lipid β-oxidation for diabetic nephropathy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 463, Issue 3, 31 July 2015, Pages 364-369
Journal: Biochemical and Biophysical Research Communications - Volume 463, Issue 3, 31 July 2015, Pages 364-369
نویسندگان
Wei Xin, Xu Zhao, Lei Liu, Ying Xu, Zhaoping Li, Liyong Chen, Xiaojie Wang, Fan Yi, Qiang Wan,