Role of TSC-mTOR pathway in diabetic nephropathy

被引:54
作者
Inoki, Ken [1 ,2 ]
机构
[1] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48108 USA
[2] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
关键词
Diabetes; mTOR; TSC; Rapamycin; Diabetic nephropathy;
D O I
10.1016/j.diabres.2008.09.028
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
TsC-mTOR signaling plays a crucial role in the regulation of cell growth and survival control. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase that forms two distinct functional complexes, termed TOR complex 1 (TORC1) and TORC2, respectively. TORC1 is a rapamycin-sensitive complex and regulates a wide array of cellular processes including translation, transcription, and autophagy. Tuberous sclerosis complex (TSC) gene products, TSC1 and TSC2 are tumor suppressors and specifically suppress TORC1 activity. Mutation of either TSC1 or TSC2 causes TSC disease, which is characterized by formation of hamartomas in multiple organs. Although the role of TSC-mTOR pathway in tumor and cancer development has been extensively studied, more recent studies have indicated a role for mTOR function in appetite, memory, aging, and energy metabolism. Dysregulation of the TSC-mTOR pathway may cause not only tumor development but also metabolic disorders such as diabetes and its complications. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:S59 / S62
页数:4
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