The cellular and molecular mechanisms of diabetic complications

被引：255

作者：

King, GL

Brownlee, M

机构：

[1] HARVARD UNIV,SCH MED,DEPT INTERNAL MED,BOSTON,MA

[2] BRIGHAM & WOMENS HOSP,DEPT INTERNAL MED,BOSTON,MA 02115

[3] ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10467

[4] ALBERT EINSTEIN COLL MED,DIABET RES CTR,BRONX,NY 10467

来源：

ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA | 1996年 / 25卷 / 02期

关键词：

D O I：

10.1016/S0889-8529(05)70324-8

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：

Hyperglycemia-induced mechanisms that may induce diabetic vascular dysfunction include increased polyol pathway flux, altered cellular redox state, increased formation of diacylglycerol, the subsequent activation of protein kinase C isoforms, and accelerated nonenzymatic formation of advanced glycation end products. Growth factor abnormalities and insulin resistance also may have a role.

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页码：255 / &

页数：17

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