The DOI matches its Crossref record; 128 of the 128 references it cites were found in a registry or an index.
The Role of Inflammatory Cytokines in Diabetic Nephropathy
Abstract
Cytokines act as pleiotropic polypeptides regulating inflammatory and immune responses through actions on cells. They provide important signals in the pathophysiology of a range of diseases, including diabetes mellitus. Chronic low-grade inflammation and activation of the innate immune system are closely involved in the pathogenesis of diabetes and its microvascular complications. Inflammatory cytokines, mainly IL-1, IL-6, and IL-18, as well as TNF-alpha, are involved in the development and progression of diabetic nephropathy. In this context, cytokine genetics is of special interest to combinatorial polymorphisms among cytokine genes, their functional variations, and general susceptibility to diabetic nephropathy. Finally, the recognition of these molecules as significant pathogenic mediators in diabetic nephropathy leaves open the possibility of new potential therapeutic targets.
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Cites
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Cited by
Mechanisms of Diabetic Complications
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AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms
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Toll-Like Receptor 4 Promotes Tubular Inflammation in Diabetic Nephropathy
Lin, M., Yiu, W. H., Wu, H. J., Chan, L. Y. Y., Leung, J. C. K., Au, W. S., Chan, K. W., Lai, K. N., & Tang, S. C. W. (2012) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010111210 · Cited by 386
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Inflammation in obesity and diabetes: islet dysfunction and therapeutic opportunity
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Metadata
- Authors
- Navarro-González, J. F., & Mora-Fernández, C.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2008-03
- Volume
- 19
- Issue
- 3
- Pages
- 433-442
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2108192985
- Cited by
- 932
- References
- 128
- FWCI
- 23.52
- Type
- journal article
- Language
- en
- Open access
- closed
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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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