期刊文献+

DHCR24表达的调控及其与丙型肝炎病毒感染的研究进展

Regulation of DHCR24 expression and its progress with HCV infection
下载PDF
导出
摘要 24-脱氢胆固醇还原酶(3β-hydroxysterolΔ~24-reductase,DHCR24)可催化链甾醇转化为胆固醇,参与多种脂代谢异常相关疾病(肝病、心血管疾病和链甾醇血症等)的发生发展。丙型肝炎病毒(hepatitis C virus,HCV)感染导致肝脏脂代谢紊乱以及肝脏炎症,并且可通过增强子诱导DHCR24表达增多[1-2]。 3β-hydroxysterol Δ^(24)-reductase( DHCR24) catalyzes the conversion of desmosterol to cholesterol and in turn affects lipid metabolism. DHCR24 is a multifunctional protein with enzymatic activity, antioxidant stress,scavenging of reactive oxygen species( ROS) and anti-apoptotic effects. Hepatitis C virus( HCV) infection results in severe oxidative stress which is correlated closely with fatty liver,liver cirrhosis,liver cancer and a series of liver diseases.Recent studies have shown that DHCR24 expression is regulated by various factors such as sterols,hormones and growth factors,and the expression of DHCR24 is significantly increased after HCV infection. In-depth study of the function and regulation of DHCR24 and its relationship with disease can be help to further discover and understand the pathogenesis,and contribute to early diagnosis and treatment of disease. This review summarizes the regulation of DHCR24 expression and its progress with HCV infection.
作者 张友浦 王敏 罗光华 张晓膺 ZHANG You-pu;WANG Min;LUO Guang-hua;ZHANG Xiao-ying(Department of Cardio-Thoracic Surgery;Comprehensive Laboratory,Third Affiliated Hospital of SoochowUniversity,Changzhou 213000,China)
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2018年第7期1333-1338,1344,共7页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助项目(No.81370372)
关键词 DHCR24 丙型肝炎病毒 激素 转录调节 DHCR24 Hepatitis C virus Hormone Transcription regulation
  • 相关文献

参考文献2

二级参考文献66

  • 1Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer's disease. Neurobiol Aging 2000, 21: 383-421.
  • 2Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer's disease. Alzhei- mers Dement 2007, 3: 186-191.
  • 3De Felice FG. Alzheimer's disease and insulin resistance: trans- lating basic science into clinical applications. J Clin Invest 2013, 123: 531-539.
  • 4Xiong H, Callaghan D, Jones A, Walker DG, Lue LF, Beach TG, et al. Cholesterol retention in Alzheimer's brain is responsible for high beta- and gamma-secretase activities and Abeta production. Neurobiol Dis 2008, 29: 422-437..
  • 5Selkoe DJ. Alzheimer's disease: genes, proteins, and therapy. Physiol Rev 2001, 81: 741-766.
  • 6Soriano S, Lu DC, Chandra S, Pietrzik CU, Koo EH. The amy- loidogenic pathway of amyloid precursor protein (APP) is inde- pendent of its cleavage by caspases. J Biol Chem 2001, 276: 29045-29050.
  • 7Gouras GK, Tsai J, Naslund J, Vincent B, Edgar M, Checler F, et al. Intraneuronal Abeta42 accumulation in human brain. Am J Pathol 2000, 156: 15-20.
  • 8LaFerla FM, Green KN, Oddo S. Intracellular amyloid-beta in Alzheimer's disease. Nat Rev Neurosci 2007, 8: 499-509.
  • 9Annaert W, De Strooper B. A cell biological perspective on Alzheimer's disease. Annu Rev Cell Dev Biol 2002, 18: 25-51.
  • 10Sato M, Murakami K, Uno M, Nakagawa Y, Katayama S, Akagi K, et al. Site-specific inhibitory mechanism for amyloid beta42 aggregation by catechol-type flavonoids targeting the Lys resi- dues. J Biol Chem 2013, 288: 23212-23224.

共引文献22

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部