The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Diabetic complications and dysregulated innate immunity
Open accessAbstract
Diabetes mellitus is a metabolic disorder that leads to the development of a number of complications. The etiology of each diabetic complication is undoubtedly multifactorial. We will focus on one potential component that may be common in many diabetic complications, dysregulation of innate immunity associated with an increased inflammatory response. High glucose levels lead to shunting through the polyol pathway, an increase in diacylglycerol which activates protein kinase C, an increase in the release of electrons that react with oxygen molecules to form superoxides, and the non-enzymatic glycosylation of proteins that result in greater formation of advanced glycation end products. Each of these can lead to aberrant cell signalling that affects innate immunity for example, by activating the MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. This may be a common feature of several complications including periodontal disease, atherosclerosis, nephropathy, impaired healing and retinopathy. These complications are frequently associated with increased expression of inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species. Cause and effect relationship between dysregulation of key components of innate immunity and diabetic complications in many instances have been demonstrated with the use of cytokine blockers and antioxidants.
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Cites
Biochemistry and molecular cell biology of diabetic complications
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Cited by
Diabetes and Its Effect on Bone and Fracture Healing
Jiao, H., Xiao, E., & Graves, D. T. (2015) · Current Osteoporosis Reports · doi:10.1007/s11914-015-0286-8 · Cited by 522
Self-citationA review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes
Taylor, J. J., Preshaw, P. M., & Lalla, E. (2013) · Journal of Clinical Periodontology · doi:10.1111/jcpe.12059 · Cited by 425
Diabetes mellitus related bone metabolism and periodontal disease
Wu, Y.-Y., Xiao, E., & Graves, D. T. (2015) · International Journal of Oral Science · doi:10.1038/ijos.2015.2 · Cited by 310
Self-citationPTSD is associated with an excess of inflammatory immune activities
Gill, J. M., Saligan, L., Woods, S., & Page, G. (2009) · Perspectives in Psychiatric Care · doi:10.1111/j.1744-6163.2009.00229.x · Cited by 271
Low cortisol, high DHEA, and high levels of stimulated TNF‐α, and IL‐6 in women with PTSD
Gill, J., Vythilingam, M., & Page, G. G. (2008) · Journal of Traumatic Stress · doi:10.1002/jts.20372 · Cited by 240
Metadata
- Authors
- Graves, D.
- Venue
- Frontiers in Bioscience
- Publisher
- IMR Press
- Published
- 2008
- Volume
- 13
- Issue
- 13
- Pages
- 1227
- ISSN
- 1093-4715 (ISSN-L)
- 1093-9946
- DOI
- 10.2741/2757
- OpenAlex
- W1536052747
- Cited by
- 249
- References
- 10
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- bronze
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Data sources
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.
