Endothelial Dysfunction in Diabetes Mellitus: Possible Involvement of Endoplasmic Reticulum Stress?

被引:96
作者
Basha, Basma [1 ]
Samuel, Samson Mathews [1 ]
Triggle, Chris R. [1 ]
Ding, Hong [1 ]
机构
[1] Qatar Fdn, Weill Cornell Med Coll Qatar, Dept Pharmacol, Doha, Qatar
关键词
UNFOLDED PROTEIN RESPONSE; C-REACTIVE PROTEIN; INCREASED OXIDATIVE STRESS; NITRIC-OXIDE SYNTHASE; HIGH-GLUCOSE; ER STRESS; SUPEROXIDE-PRODUCTION; TNF-ALPHA; VASCULAR COMPLICATIONS; TRANSLATIONAL CONTROL;
D O I
10.1155/2012/481840
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The vascular complications of diabetes mellitus impose a huge burden on the management of this disease. The higher incidence of cardiovascular complications and the unfavorable prognosis among diabetic individuals who develop such complications have been correlated to the hyperglycemia-induced oxidative stress and associated endothelial dysfunction. Although antioxidants may be considered as effective therapeutic agents to relieve oxidative stress and protect the endothelium, recent clinical trials involving these agents have shown limited therapeutic efficacy in this regard. In the recent past experimental evidence suggests that endoplasmic reticulum (ER) stress in the endothelial cells might be an important contributor to diabetes-related vascular complications. The current paper contemplates the possibility of the involvement of ER stress in endothelial dysfunction and diabetes-associated vascular complications.
引用
收藏
页数:14
相关论文
共 135 条
[11]   Intracellular signaling by the unfolded protein response [J].
Bernales, Sebastian ;
Papa, Feroz R. ;
Walter, Peter .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 2006, 22 :487-508
[12]   Glucose enhances expression of TRPC1 and calcium entry in endothelial cells [J].
Bishara, N. B. ;
Ding, H. .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2010, 298 (01) :H171-H178
[13]   The importance of endothelin-1 for vascular dysfunction in cardiovascular disease [J].
Boehm, Felix ;
Pernow, John .
CARDIOVASCULAR RESEARCH, 2007, 76 (01) :8-18
[14]   A selective inhibitor-of eIF2α dephosphorylation protects cells from ER stress [J].
Boyce, M ;
Bryant, KF ;
Jousse, C ;
Long, K ;
Harding, HP ;
Scheuner, D ;
Kaufman, RJ ;
Ma, DW ;
Coen, DM ;
Ron, D ;
Yuan, JY .
SCIENCE, 2005, 307 (5711) :935-939
[15]   No Superoxide-No Stress? Nox4, the Good NADPH Oxidase! [J].
Brandes, Ralf P. ;
Takac, Ina ;
Schroeder, Katrin .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2011, 31 (06) :1255-1257
[16]   Hyperglycemia Induces a Dynamic Cooperativity of Histone Methylase and Demethylase Enzymes Associated With Gene-Activating Epigenetic Marks That Coexist on the Lysine Tail [J].
Brasacchio, Daniella ;
Okabe, Jun ;
Tikellis, Christos ;
Balcerczyk, Aneta ;
George, Prince ;
Baker, Emma K. ;
Calkin, Anna C. ;
Brownlee, Michael ;
Cooper, Mark E. ;
El-Osta, Assam .
DIABETES, 2009, 58 (05) :1229-1236
[17]   Regulation of apoptosis by endoplasmic reticulum pathways [J].
Breckenridge, DG ;
Germain, M ;
Mathai, JP ;
Nguyen, M ;
Shore, GC .
ONCOGENE, 2003, 22 (53) :8608-8618
[18]   Hyperglycemic switch from mitochondrial nitric oxide to superoxide production in endothelial cells [J].
Brodsky, SV ;
Gao, SJ ;
Li, H ;
Goligorsky, MS .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2002, 283 (05) :H2130-H2139
[19]   Growth arrest and DNA damage-inducible protein GADD34 targets protein phosphatase 1α to the endoplasmic reticulum and promotes dephosphorylation of the α subunit of eukaryotic translation initiation factor 2 [J].
Brush, MH ;
Weiser, DC ;
Shenolikar, S .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (04) :1292-1303
[20]   Hyperglycemia-induced reactive oxygen species toxicity to endothelial cells is dependent on paracrine mediators [J].
Busik, Julia V. ;
Mohr, Susanne ;
Grant, Maria B. .
DIABETES, 2008, 57 (07) :1952-1965