Literature DB >> 1644256

Glucose and diabetic vascular disease.

N B Ruderman1, J R Williamson, M Brownlee.   

Abstract

The central therapeutic problem in diabetes mellitus is prevention and treatment of the chronic vascular disease associated with this disorder. Prolonged exposure to hyperglycemia is the primary factor associated with the development of diabetes-specific microvascular disease, and the relationship between deranged glucose metabolism and arterial disease is complicated by many other factors that influence atherogenesis in nondiabetics. Until relatively recently, knowledge about diabetic vascular disease was limited mainly to clinical description. New information about abnormal vascular physiology, ultrastructure, biochemistry, cell biology, and molecular biology now makes it possible to understand in an integrated fashion the major specific mechanisms by which hyperglycemia damages diabetic vessels. Continued progress in this area will further optimize the development of safe and effective drugs for the treatment of diabetic vascular disease.

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Year:  1992        PMID: 1644256     DOI: 10.1096/fasebj.6.11.1644256

Source DB:  PubMed          Journal:  FASEB J        ISSN: 0892-6638            Impact factor:   5.191


  75 in total

1.  An explorative analysis of secretory receptor for advanced glycation endproducts in primary focal segmental glomerulosclerosis.

Authors:  Harin Rhee; Sang Heon Song; Ihm Soo Kwak; Il Young Kim; Eun Young Seong; Dong Won Lee; Soo Bong Lee
Journal:  Clin Exp Nephrol       Date:  2012-08       Impact factor: 2.801

Review 2.  Role of nitrosative stress in the pathogenesis of diabetic vascular dysfunction.

Authors:  Csaba Szabo
Journal:  Br J Pharmacol       Date:  2009-02-06       Impact factor: 8.739

3.  Studies on advanced glycation end products by recent mass spectrometric techniques.

Authors:  A Lapolla; D Fedele; P Traldi
Journal:  Amino Acids       Date:  1994-02       Impact factor: 3.520

4.  Nuclear factor kappa B inhibition improves conductance artery function in type 2 diabetic mice.

Authors:  Modar Kassan; Soo-Kyoung Choi; Maria Galán; Mohamed Trebak; Souad Belmadani; Khalid Matrougui
Journal:  Diabetes Metab Res Rev       Date:  2015-01       Impact factor: 4.876

5.  Cultured retinal capillary pericytes die by apoptosis after an abrupt fluctuation from high to low glucose levels: a comparative study with retinal capillary endothelial cells.

Authors:  W Li; X Liu; M Yanoff; S Cohen; X Ye
Journal:  Diabetologia       Date:  1996-05       Impact factor: 10.122

6.  Activation of AKT by O-linked N-acetylglucosamine induces vascular calcification in diabetes mellitus.

Authors:  Jack M Heath; Yong Sun; Kaiyu Yuan; Wayne E Bradley; Silvio Litovsky; Louis J Dell'Italia; John C Chatham; Hui Wu; Yabing Chen
Journal:  Circ Res       Date:  2014-02-13       Impact factor: 17.367

7.  Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.

Authors:  A M Schmidt; O Hori; J X Chen; J F Li; J Crandall; J Zhang; R Cao; S D Yan; J Brett; D Stern
Journal:  J Clin Invest       Date:  1995-09       Impact factor: 14.808

8.  Retinal angiogenesis in the Ins2(Akita) mouse model of diabetic retinopathy.

Authors:  Zongchao Han; Junjing Guo; Shannon M Conley; Muna I Naash
Journal:  Invest Ophthalmol Vis Sci       Date:  2013-01-17       Impact factor: 4.799

9.  Diabetes reduces the cholesterol exporter ABCA1 in mouse macrophages and kidneys.

Authors:  Chongren Tang; Jenny E Kanter; Karin E Bornfeldt; Renee C Leboeuf; John F Oram
Journal:  J Lipid Res       Date:  2009-11-23       Impact factor: 5.922

10.  N(epsilon)-(Carboxymethyl)lysine and Coronary Atherosclerosis-Associated Low Density Lipoprotein Abnormalities in Type 2 Diabetes: Current Status.

Authors:  Khaled A Ahmed; Sekaran Muniandy; Ikram S Ismail
Journal:  J Clin Biochem Nutr       Date:  2008-12-27       Impact factor: 3.114

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