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Diabetic Cardiovascular Disease Induced by Oxidative Stress

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2015 Oct 30
PMID 26512646
Citations 147
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Abstract

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality among patients with diabetes mellitus (DM). DM can lead to multiple cardiovascular complications, including coronary artery disease (CAD), cardiac hypertrophy, and heart failure (HF). HF represents one of the most common causes of death in patients with DM and results from DM-induced CAD and diabetic cardiomyopathy. Oxidative stress is closely associated with the pathogenesis of DM and results from overproduction of reactive oxygen species (ROS). ROS overproduction is associated with hyperglycemia and metabolic disorders, such as impaired antioxidant function in conjunction with impaired antioxidant activity. Long-term exposure to oxidative stress in DM induces chronic inflammation and fibrosis in a range of tissues, leading to formation and progression of disease states in these tissues. Indeed, markers for oxidative stress are overexpressed in patients with DM, suggesting that increased ROS may be primarily responsible for the development of diabetic complications. Therefore, an understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of diabetes-induced CVD. The current review focuses on the relationship between diabetes-induced CVD and oxidative stress, while highlighting the latest insights into this relationship from findings on diabetic heart and vascular disease.

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References
1.
Tousoulis D, Psaltopoulou T, Androulakis E, Papageorgiou N, Papaioannou S, Oikonomou E . Oxidative stress and early atherosclerosis: novel antioxidant treatment. Cardiovasc Drugs Ther. 2014; 29(1):75-88. DOI: 10.1007/s10557-014-6562-5. View

2.
Dai D, Chen T, Szeto H, Nieves-Cintron M, Kutyavin V, Santana L . Mitochondrial targeted antioxidant Peptide ameliorates hypertensive cardiomyopathy. J Am Coll Cardiol. 2011; 58(1):73-82. PMC: 3742010. DOI: 10.1016/j.jacc.2010.12.044. View

3.
Hinokio Y, Suzuki S, Hirai M, Suzuki C, Suzuki M, Toyota T . Urinary excretion of 8-oxo-7, 8-dihydro-2'-deoxyguanosine as a predictor of the development of diabetic nephropathy. Diabetologia. 2002; 45(6):877-82. DOI: 10.1007/s00125-002-0831-8. View

4.
Fleenor B, Seals D, Zigler M, Sindler A . Superoxide-lowering therapy with TEMPOL reverses arterial dysfunction with aging in mice. Aging Cell. 2011; 11(2):269-76. PMC: 3409251. DOI: 10.1111/j.1474-9726.2011.00783.x. View

5.
Ichijo H, Nishida E, Irie K, Ten Dijke P, Saitoh M, Moriguchi T . Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways. Science. 1997; 275(5296):90-4. DOI: 10.1126/science.275.5296.90. View