Role of Hepatocyte ATF3 in NAFLD
肝细胞 ATF3 在 NAFLD 中的作用
基本信息
- 批准号:10224182
- 负责人:
- 金额:$ 45.82万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2018
- 资助国家:美国
- 起止时间:2018-08-01 至 2024-03-31
- 项目状态:已结题
- 来源:
- 关键词:3&apos Untranslated RegionsAttenuatedBile AcidsBindingBiological ProcessCatabolismCholesterolCholesterol HomeostasisCyclic AMP Response ElementDataDeveloped CountriesDevelopmentDiabetes MellitusDown-RegulationFamilyFatty LiverFibrosisGene ExpressionGenesHealthHepaticHepatocyteHigh Fat DietHomeostasisHumanInflammationInflammatory ResponseKupffer CellsLeadLipidsLiverLiver CirrhosisLiver diseasesMediatingMetabolic stressMicroRNAsMusObese MiceObesityPathogenesisPatientsPharmacologyPlayPrimary carcinoma of the liver cellsRegulationRepressionRisk FactorsRoleSignal PathwayTriglyceride MetabolismTriglyceridesUntranslated RNAactivating transcription factoractivating transcription factor 3chronic liver diseasediabeticimprovedknock-downlipid metabolismliver injuryloss of functionmacrophagemembernon-alcoholic fatty liver diseasenonalcoholic steatohepatitisnoveloverexpressionpreventstellate celltherapeutic targettranscription factortreatment strategywestern diet
项目摘要
Project Summary
Project Summary: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in
developed countries, which ranges from simple steatosis to non-alcoholic steatohepatitis (NASH). So far, the
mechanisms underlying the development of NAFLD is poorly understood. Activating transcription factor 3
(ATF3) is a member of the ATF/cAMP response element-binding (ATF/CREB) family of transcription factors,
and inhibits inflammatory response in macrophages. Until now, nothing has been known about the role of
hepatic ATF3 in lipid metabolism. Our preliminary studies have shown that hepatic ATF3 expression is
markedly reduced under common metabolic stress. Over-expression of ATF3 in the liver improves lipid
homeostasis whereas loss of hepatic ATF3 has opposite effects. In this project, we will investigate whether and
how hepatic ATF3 regulates the development of NAFLD. We will use both gain- and loss-of-function
approaches to complete this project. Completion of the proposed studies may help identify hepatocyte ATF3 as
a key regulator of lipid metabolism and the development of NAFLD.
项目概要
项目摘要:非酒精性脂肪肝病(NAFLD)是最常见的慢性肝病
发达国家,其范围从单纯性脂肪变性到非酒精性脂肪性肝炎(NASH)。到目前为止,
NAFLD 发展的潜在机制尚不清楚。激活转录因子3
(ATF3) 是转录因子 ATF/cAMP 反应元件结合 (ATF/CREB) 家族的成员,
并抑制巨噬细胞的炎症反应。到目前为止,人们对它的作用还一无所知
肝脏ATF3在脂质代谢中的作用。我们的初步研究表明肝脏 ATF3 表达
在常见的代谢应激下显着降低。肝脏中 ATF3 的过度表达可改善血脂
肝脏 ATF3 的丧失会产生相反的影响。在这个项目中,我们将调查是否和
肝脏 ATF3 如何调节 NAFLD 的发展。我们将同时使用功能获得和功能丧失
完成该项目的方法。完成拟议的研究可能有助于将肝细胞 ATF3 确定为
脂质代谢和 NAFLD 发展的关键调节因子。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Yanqiao Zhang其他文献
Yanqiao Zhang的其他文献
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{{ truncateString('Yanqiao Zhang', 18)}}的其他基金
Hepatic FOXA3 Links NAFLD to Atherosclerosis
肝脏 FOXA3 将 NAFLD 与动脉粥样硬化联系起来
- 批准号:
10364733 - 财政年份:2019
- 资助金额:
$ 45.82万 - 项目类别:
Hepatic FOXA3 Links NAFLD to Atherosclerosis
肝脏 FOXA3 将 NAFLD 与动脉粥样硬化联系起来
- 批准号:
9891056 - 财政年份:2019
- 资助金额:
$ 45.82万 - 项目类别:
Identification of Novel Genes/Pathways That Regulate Atherogenesis
调节动脉粥样硬化形成的新基因/途径的鉴定
- 批准号:
10199006 - 财政年份:2018
- 资助金额:
$ 45.82万 - 项目类别:
Mechanisms Underlying the Pathogenesis of Non-alcoholic Fatty Liver Disease
非酒精性脂肪肝发病机制
- 批准号:
10594713 - 财政年份:2015
- 资助金额:
$ 45.82万 - 项目类别:
Mechanisms Underlying the Pathogenesis of Non-alcoholic Fatty Liver Disease
非酒精性脂肪肝发病机制
- 批准号:
8884995 - 财政年份:2015
- 资助金额:
$ 45.82万 - 项目类别:
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