Haeme oxygenase signalling pathway: implications for cardiovascular disease

被引:65
|
作者
Fredenburgh, Laura E. [1 ]
Merz, Allison A. [2 ]
Cheng, Susan [2 ,3 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA
[2] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med, Boston, MA 02115 USA
[3] Framingham Heart Dis Epidemiol Study, Framingham, MA USA
关键词
Heme oxygenase pathway; Carbon monoxide; Bilirubin; Biliverdin; Cardiovascular disease; CORONARY-ARTERY-DISEASE; GENE PROMOTER POLYMORPHISM; PROTEIN-KINASE PATHWAY; GT-REPEAT POLYMORPHISM; SMOOTH-MUSCLE-CELLS; PANCREATIC BETA-CELLS; ATHEROSCLEROTIC LESION FORMATION; SPONTANEOUSLY HYPERTENSIVE-RATS; ENHANCES INSULIN SENSITIVITY; VASCULAR ENDOTHELIAL-CELLS;
D O I
10.1093/eurheartj/ehv114
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Evidence now points to the haeme oxygenase (HO) pathway as a possible actor in modulating risk for cardiovascular disease (CVD). In particular, the HO pathway may represent a key endogenous modulator of oxidative, inflammatory, and cytotoxic stress while also exhibiting vasoregulatory properties. In this review, we summarize the accumulating experimental and emerging clinical data indicating how activity of the HO pathway and its products may play a role in mechanisms underlying the development of CVD. We also identify gaps in the literature to date and suggest future directions for investigation. Because HO pathway activity can be influenced not only by genetic traits and environmental stimuli but also by a variety of existing pharmacologic interventions, the pathway could serve as a prime target for reducing the overall burden of CVD. Further work is needed to determine the role of HO pathway products as possible prognostic markers of risk for clinical CVD events and the extent to which therapeutic augmentation or inhibition of HO pathway activity could serve to modify CVD risk.
引用
收藏
页码:1512 / U92
页数:11
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