Insulin Resistance, Hyperglycemia, and Atherosclerosis

被引：632
|
作者：
Bornfeldt, Karin E. [2 ]
Tabas, Ira [1 ,3 ,4 ]
机构：
[1] Columbia Univ, Dept Med, New York, NY 10032 USA
[2] Univ Washington, Dept Pathol, Diabet & Obes Ctr Excellence, Seattle, WA 98109 USA
[3] Columbia Univ, Dept Anat & Cell Biol, New York, NY 10032 USA
[4] Columbia Univ, Dept Physiol & Cellular Biophys, New York, NY 10032 USA
来源：
CELL METABOLISM | 2011年 / 14卷 / 05期
关键词：
ENDOPLASMIC-RETICULUM STRESS; GLYCATION END-PRODUCTS; SMOOTH-MUSCLE; CARDIOVASCULAR-DISEASE; ACCELERATES ATHEROSCLEROSIS; DIABETIC ATHEROSCLEROSIS; GENE-EXPRESSION; GLUCOSE CONTROL; CLINICAL-TRIAL; RECEPTOR;
D O I：
10.1016/j.cmet.2011.07.015
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Progress in preventing atherosclerotic coronary artery disease (CAD) has been stalled by the epidemic of type 2 diabetes. Further advances in this area demand a thorough understanding of how two major features of type 2 diabetes, insulin resistance and hyperglycemia, impact atherosclerosis. Insulin resistance is associated with systemic CAD risk factors, but increasing evidence suggests that defective insulin signaling in atherosclerotic lesional cells also plays an important role. The role of hyperglycemia in CAD associated with type 2 diabetes is less clear. Understanding the mechanisms whereby type 2 diabetes exacerbates CAD offers hope for new therapeutic strategies to prevent and treat atherosclerotic vascular disease.
引用
收藏
页码：575 / 585
页数：11
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