The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
How hyperglycemia promotes atherosclerosis: molecular mechanisms
Open accessAbstract
Both type I and type II diabetes are powerful and independent risk factors for coronary artery disease (CAD), stroke, and peripheral arterial disease. Atherosclerosis accounts for virtually 80% of all deaths among diabetic patients. Prolonged exposure to hyperglycemia is now recognized a major factor in the pathogenesis of atherosclerosis in diabetes. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerate the atherosclerotic process. Animal and human studies have elucidated three major mechanisms that encompass most of the pathological alterations observed in the diabetic vasculature: 1) Nonenzymatic glycosylation of proteins and lipids which can interfere with their normal function by disrupting molecular conformation, alter enzymatic activity, reduce degradative capacity, and interfere with receptor recognition. In addition, glycosylated proteins interact with a specific receptor present on all cells relevant to the atherosclerotic process, including monocyte-derived macrophages, endothelial cells, and smooth muscle cells. The interaction of glycosylated proteins with their receptor results in the induction of oxidative stress and proinflammatory responses 2) oxidative stress 3) protein kinase C (PKC) activation with subsequent alteration in growth factor expression. Importantly, these mechanisms may be interrelated. For example, hyperglycemia-induced oxidative stress promotes both the formation of advanced glycosylation end products and PKC activation.
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Cites
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Background
Cited by
Grundy, S. M., Cleeman, J. I., Daniels, S. R., Donato, K. A., Eckel, R. H., Franklin, B. A., Gordon, D. J., Krauss, R. M., Savage, P. J., Smith, S. C., et al. (2005) · Circulation · doi:10.1161/circulationaha.105.169404 · Cited by 11,961
Oxidative stress and atherosclerosis
Singh, U., & Jialal, I. (2006) · Pathophysiology · doi:10.1016/j.pathophys.2006.05.002 · Cited by 490
Dietary Advanced Glycation End Products and Aging
Luevano-Contreras, C., & Chapman-Novakofski, K. (2010) · Nutrients · doi:10.3390/nu2121247 · Cited by 396
The cardio-renal-metabolic connection: a review of the evidence
Marassi, M., & Fadini, G. P. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01937-x · Cited by 386
Metformin Decreases Intracellular Production of Reactive Oxygen Species in Aortic Endothelial Cells
Ouslimani, N., Peynet, J., Bonnefont-Rousselot, D., Thérond, P., Legrand, A., & Beaudeux, J.-L. (2005) · Metabolism · doi:10.1016/j.metabol.2005.01.029 · Cited by 204
Metadata
- Authors
- Aronson, D., & Rayfield, E. J.
- Venue
- Cardiovascular Diabetology
- Published
- 2002-04-08
- Volume
- 1
- Issue
- 1
- Pages
- 1-1
- ISSN
- 1475-2840 (ISSN-L)
- OpenAlex
- W2127764309
- Cited by
- 504
- References
- 9
- FWCI
- 10.61
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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