کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5513167 | 1540979 | 2017 | 56 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
1,25-Dihydroxyvitamin-D3 prevents the development of diabetic cardiomyopathy in type 1 diabetic rats by enhancing autophagy via inhibiting the β-catenin/TCF4/GSK-3β/mTOR pathway
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کلمات کلیدی
mTORSTZGSK-3βLiClBAFTSCTcf4VDR1,25D3GFPT-cell factor/lymphoid enhancer factorDBPCVFSBPDCM1,25-dihydroxyvitamin D3 - 1،25-دی هیدروکسوییتامین D325(OH)D - 25 (OH) DPCA - PCAAutophagy - اتوفاژیstreptozotocin - استرپتوزوتوسینbafilomycin A1 - بافیلومایسین A1Type 1 diabetes - دیابت نوع۱Heart rate - ضربان قلبtibia length - طول تیبیاdiastolic blood pressure - فشار خون دیاستولیکsystolic blood pressure - فشار خون سیستولیکmean arterial pressure - فشار متوسط شریانیlithium chloride - لیتیم کلریدmap - نقشهmammalian target of rapamycin - هدف پستانداران رپامایسینbody weight - وزن بدنHeart weight - وزن قلبVitamin D - ویتامین دیgreen fluorescent protein - پروتئین فلورسنت سبزdiabetic cardiomyopathy - کاردیومیوپاتی دیابتی یا بیماری قلبی دیابتیcollagen volume fraction - کسر حجم کلاژنventricular ejection fraction - کسری تخلیه بطنیChloroquine - کلروکین Tuberous sclerosis complex - کمپلکس توبروس اسکلروزیسfractional shortening - کوتاه کردن کسریhigh glucose - گلوکز بالا یا قند بالاGlycogen synthase kinase-3β - گلیکوزین سنتاز کیناز 3βVitamin D receptor - گیرنده ویتامین D
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Diabetic cardiomyopathy (DCM) can increase the risk of heart failure and death in diabetic patients. However, no effective approaches are available to prevent its progression and development. Studies have shown that vitamin D is greatly implicated in cardiac hypertrophy and fibrosis, and there is a high prevalence of vitamin D deficiency in diabetic patients. In this study, we investigated whether 1,25-Dihydroxyvitamin-D3 (1,25D3) can improve DCM through a vitamin D receptor (VDR)-dependent mechanism associated with autophagy and the β-catenin/T-cell factor/lymphoid enhancer factor (TCF4)/glycogen synthase kinase-3β (GSK-3β)/mammalian target of rapamycin (mTOR) pathway. In this study, streptozotocin (STZ)-induced type 1 diabetic rats were established and were treated with 1,25D3 and/or chloroquine and/or VDR gene silencing for 8 weeks before being sacrificed. Compared with untreated diabetic rats, 1,25D3 partly attenuated the myocardial hypertrophy and interstitial fibrosis, improved cardiac function and restored the impaired cardiac autophagy in diabetic rats, all of which were reversed by silencing the VDR gene in diabetic rats. In high-glucose cultured H9C2 cells, 1,25D3 increased autophagy in a dose-dependent manner. Besides, the β-catenin/TCF4/GSK-3β and mTOR signaling were activated both in diabetic rats and in high-glucose cultured H9C2 cells. Treatment with 1,25D3 inhibited the β-catenin/TCF4/GSK-3β and mTOR signaling in H9C2 cells, whereas co-treatment with lithium chloride (LiCl) reversed this situation and abolished the beneficial effect of 1,25D3 on autophagy. These data suggest that 1,25D3 may improve DCM in type 1 diabetic rats by modulating autophagy through the β-catenin/TCF4/GSK-3β and mTOR pathway. Vitamin D may exist as a new therapeutic target for the treatment of DCM.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 168, April 2017, Pages 71-90
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 168, April 2017, Pages 71-90
نویسندگان
Huili Wei, Hua Qu, Hang Wang, Baolan Ji, Yao Ding, Dan Liu, Yang Duan, Huimin Liang, Chuan Peng, Xiaoqiu Xiao, Huacong Deng,