کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8537030 | 1560926 | 2017 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Targeting nuclear receptors for the treatment of fatty liver disease
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کلمات کلیدی
AMPKACACbACACAacyl-CoA oxidase 1ACADMαSMACDCAACOX1Cpt1aABCALTCCl4AFB1 - AFB 1ALD - آدرنولکودیستروفیAflatoxin B1 - آفلاتوکسین B1Alanine aminotransferase - آلانین آمینوترانسفرازacetyl-CoA carboxylase α - اتیل کوآ آر کربوکسیلااز αalcoholic steatohepatitis - استاتو هپاتیت الکلیChenodeoxycholic acid - اسید ChenodeoxycholicBile acid - اسید صفراویα-smooth muscle actin - اکتین عضله آلفا صافalcoholic liver disease - بیماری کبدی الکلیATP-binding cassette transporter - حمل کننده کاسه اتصال ATPAsh - خاکسترMedium-chain acyl-CoA dehydrogenase - زنجیره آلییل CoA dehydrogenase زنجیره متوسطCAR - ماشینadenosine monophosphate-activated protein kinase - پروتئین کیناز فعال شده با آدنوزین مونوفسفاتCarbon tetrachloride - کربن تتراکلریدconstitutive androstane receptor - گیرنده آندروستان پایدار
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
چکیده انگلیسی
Ligand-activated nuclear receptors, including peroxisome proliferator-activated receptor alpha (PPARα), pregnane X receptor, and constitutive androstane receptor, were first identified as key regulators of the responses against chemical toxicants. However, numerous studies using mouse disease models and human samples have revealed critical roles for these receptors and others, such as PPARβ/δ, PPARγ, farnesoid X receptor (FXR), and liver X receptor (LXR), in maintaining nutrient/energy homeostasis in part through modulation of the gut-liver-adipose axis. Recently, disorders associated with disrupted nutrient/energy homeostasis, e.g., obesity, metabolic syndrome, and non-alcoholic fatty liver disease (NAFLD), are increasing worldwide. Notably, in NAFLD, a progressive subtype exists, designated as non-alcoholic steatohepatitis (NASH) that is characterized by typical histological features resembling alcoholic steatohepatitis (ASH), and NASH/ASH are recognized as major causes of hepatitis virus-unrelated liver cirrhosis and hepatocellular carcinoma. Since hepatic steatosis is basically caused by an imbalance between fat/energy influx and utilization, abnormal signaling of these nuclear receptors contribute to the pathogenesis of fatty liver disease. Standard therapeutic interventions have not been fully established for fatty liver disease, but some new agents that activate or inhibit nuclear receptor signaling have shown promise as possible therapeutic targets. In this review, we summarize recent findings on the roles of nuclear receptors in fatty liver disease and discuss future perspectives to develop promising pharmacological strategies targeting nuclear receptors for NAFLD/NASH.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology & Therapeutics - Volume 179, November 2017, Pages 142-157
Journal: Pharmacology & Therapeutics - Volume 179, November 2017, Pages 142-157
نویسندگان
Naoki Tanaka, Toshifumi Aoyama, Shioko Kimura, Frank J. Gonzalez,