JNK regulation of hepatic manifestations of the metabolic syndrome.

JNK regulation of hepatic manifestations of the metabolic syndrome.
复制标题

DOI:
10.1016/j.tem.2010.08.010
复制
发表时间:
2010-12
影响因子:
10.9
通讯作者:
Czaja, Mark J.
Czaja, Mark J.
中科院分区:
医学1区
文献类型:
--
作者:
Czaja, Mark J.

文献摘要

参考文献

被引文献

相似文献

非酒精性脂肪性肝病(NAFLD)现在被认为是代谢综合征的重要组成部分,也是美国最流行的肝病。虽然NAFLD中脂肪变性和慢性肝损伤的发展机制仍不清楚,但最近的研究表明,c-Jun N-末端激酶(JNK)的过度活化对这一过程至关重要。这些发现,连同JNK信号转导参与代谢综合征的其他表现如肥胖和胰岛素抵抗的证据,表明JNK可能是这种疾病的新的治疗靶点。本文综述了JNK介导脂肪肝脂质蓄积和细胞损伤的研究结果,并讨论了JNK作用的可能细胞机制。
Nonalcoholic fatty liver disease (NAFLD) is now recognized as both an important component of the metabolic syndrome and the most prevalent liver disease in the United States. Although the mechanisms for development of steatosis and chronic liver injury in NAFLD remain unclear, recent investigations have indicated that overactivation of c-Jun N-terminal kinase (JNK) is critical to this process. These findings, together with evidence for the involvement of JNK signaling in other manifestations of the metabolic syndrome such as obesity and insulin resistance, have suggested that JNK may be a novel therapeutic target in this disorder. This review details findings that JNK mediates lipid accumulation and cell injury in fatty liver disease and discusses the possible cellular mechanisms of JNK actions.
DOI: 10.2337/db06-1491
发表时间: 2007-07-01
期刊: DIABETES
影响因子: 7.7
作者:
Cani, Patrice D.;Amar, Jacques;Burcelin, Remy
通讯作者: Burcelin, Remy
DOI: 10.2337/db08-0913
发表时间: 2009-03
期刊: Diabetes
影响因子: 7.7
作者:
Delibegovic M;Zimmer D;Kauffman C;Rak K;Hong EG;Cho YR;Kim JK;Kahn BB;Neel BG;Bence KK
通讯作者: Bence KK
DOI: 10.1016/j.cld.2009.07.004
发表时间: 2009-11-01
影响因子: 5.1
作者:
Kapoor, Ashwani;Sanyal, Arun J.
通讯作者: Sanyal, Arun J.
DOI: 10.1172/jci8814
发表时间: 2000-04-01
影响因子: 15.9
作者:
Leclercq, IA;Farrell, GC;Robertson, GR
通讯作者: Robertson, GR
DOI: 10.1152/ajpgi.00304.2001
发表时间: 2002-02-01
影响因子: 4.5
作者:
Liu, HL;Jones, BE;Czaja, MJ
通讯作者: Czaja, MJ