The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Proatherosclerotic Mechanisms Involving Protein Kinase C in Diabetes and Insulin Resistance
Open accessAbstract
In diabetes and insulin resistance, activation of protein kinase C (PKC) in vascular cells may be a key link between elevated plasma and tissue concentrations of glucose and nonesterified fatty acids and abnormal vascular cell signaling. Initial studies of PKC activation in diabetes focused on microvascular complications, but increasing evidence supports that PKC plays a role in several mechanisms promoting atherosclerosis. This review explains how PKC is thought to be activated in diabetes and insulin resistance through de novo synthesis of diacylglycerol. Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction; gene induction and activation of vascular NAD(P)H oxidase; endothelial nitric oxide synthase expression and function; endothelin-1 expression; growth, migration, and apoptosis of vascular smooth muscle cells; induction of adhesion molecules; and oxidized low-density lipoprotein uptake by monocyte-derived macrophages.
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Cites
Biochemistry and molecular cell biology of diabetic complications
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Interactions of Peroxynitrite, Tetrahydrobiopterin, Ascorbic Acid, and Thiols
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PKC-θ knockout mice are protected from fat-induced insulin resistance
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Cited by
Activation of Protein Kinase C Isoforms and Its Impact on Diabetic Complications
Geraldes, P., & King, G. L. (2010) · Circulation Research · doi:10.1161/circresaha.110.217117 · Cited by 985
Self-citationEndothelial dysfunction in diabetes mellitus: Molecular mechanisms and clinical implications
Tabit, C. E., Chung, W. B., Hamburg, N. M., & Vita, J. A. (2010) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-010-9134-4 · Cited by 572
Mechanisms of Disease: endothelial dysfunction in insulin resistance and diabetes
Rask-Madsen, C., & King, G. L. (2007) · Nature Clinical Practice Endocrinology & Metabolism · doi:10.1038/ncpendmet0366 · Cited by 484
Self-citationKawakami, A., Aikawa, M., Alcaide, P., Luscinskas, F. W., Libby, P., & Sacks, F. M. (2006) · Circulation · doi:10.1161/circulationaha.106.622514 · Cited by 305
Endothelial dysfunction in obesity
Engin, A. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-48382-5_15 · Cited by 255
Metadata
- Authors
- Rask-Madsen, C., & King, G. L.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2005-03
- Volume
- 25
- Issue
- 3
- Pages
- 487-496
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W1993008296
- Cited by
- 178
- References
- 14
- FWCI
- 10.22
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Rask-Madsen, C., & King, G. L. (2005). Proatherosclerotic Mechanisms Involving Protein Kinase C in Diabetes and Insulin Resistance. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/01.atv.0000155325.41507.e0
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
