Abstract
Vascular complications including impaired contractility and increased cell proliferation are the most common complications associated with diabetes. Chronic hyperglycemia appears to be an important contributing factor in this process. Various signaling pathways are implicated in diabetes/hyperglycemia-induced impaired vascular functions. Increased oxidative stress, nonenzymatic glycation, enhanced production of diacylglycerol, increased activity of protein kinase C, mitogen-activated protein kinases (MAPK), and other signaling pathways have been proposed to explain the adverse effects of hyperglycemia on vascular smooth muscle cells. Hyperglycemia-induced stimulation of the L-type Ca2+ channel via G-protein-coupled adenylyl cyclase/cAMP and phospholipase C/protein kinase C (PKC) pathways has also been shown. In addition, hyperglycemia has been reported to decrease the availability of nitric oxide and increase the formation of peroxynitrite which may contribute to all of the hemodynamic and physiological changes occurring in diabetes. G-protein/adenylyl cyclase signaling that plays an important role in the regulation of cardiovascular functions has also been reported to be impaired in diabetes and under hyperglycemic conditions. In this review, we have highlighted some key signaling pathways, including PKC, MAPK, and G-protein/adenylyl cyclase, which are altered in diabetes, and in response to hyperglycemia/oxidative stress, and discussed their contributions in the development of vascular complications.
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Keywords
- High Glucose
- Vascular Smooth Muscle Cell
- Adenylyl Cyclase
- Adenylyl Cyclase Activity
- Aortic Vascular Smooth Muscle Cell
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Srivastava, A.K., Anand-Srivastava, M.B. (2008). Role of Hyperglycemia and Redox-Induced Signaling in Vascular Complications of Diabetes. In: Srivastava, A.K., Anand-Srivastava, M.B. (eds) Signal Transduction in the Cardiovascular System in Health and Disease. Advances in Biochemistry in Health and Disease, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-09552-3_9
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