The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy
Abstract
Despite current therapies, many diabetic patients will suffer from declining renal function in association with progressive kidney inflammation. Recently, animal model studies have demonstrated that kidney macrophage accumulation is a critical factor in the development of diabetic nephropathy. However, specific anti-inflammatory strategies are not yet being considered for the treatment of patients with diabetic renal injury. This review highlights the chemokine monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine ligand 2 as a major promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. Researchers have found that diabetes induces kidney MCP-1 production and that urine MCP-1 levels can be used to assess renal inflammation in this disease. In addition, genetic deletion and molecular blocking studies in rodents have identified MCP-1 as an important therapeutic target for treating diabetic nephropathy. Evidence also suggests that a polymorphism in the human MCP-1 gene is associated with progressive kidney failure in type 2 diabetes, which may identify patients at higher risk who need additional therapy. These findings provide a strong rationale for developing specific therapies against MCP-1 and inflammation in diabetic nephropathy.
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Self-citationA Novel Polymorphism in the MCP-1 Gene Regulatory Region That Influences MCP-1 Expression
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Macrophage accumulation in human progressive diabetic nephropathy
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Blockade of CCR2 Ameliorates Progressive Fibrosis in Kidney
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Self-citation
Cited by
Macrophages: versatile players in renal inflammation and fibrosis
Tang, P. M.-K., Nikolic-Paterson, D. J., & Lan, H.-Y. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0110-2 · Cited by 1,033
Renal tubule injury: a driving force toward chronic kidney disease
Liu, B.-C., Tang, T.-T., Lv, L.-L., & Lan, H.-Y. (2018) · Kidney International · doi:10.1016/j.kint.2017.09.033 · Cited by 913
Diabetes and Kidney Disease: Role of Oxidative Stress
Jha, J. C., Banal, C., Chow, B. S. M., Cooper, M. E., & Jandeleit-Dahm, K. (2016) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6664 · Cited by 660
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Niewczas, M. A., Pavkov, M. E., Skupien, J., Smiles, A., Md Dom, Z. I., Wilson, J. M., Park, J., Nair, V., Schlafly, A., Saulnier, P.-J., et al. (2019) · Nature Medicine · doi:10.1038/s41591-019-0415-5 · Cited by 432
Metadata
- Authors
- Tesch, G. H.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2008-04
- Volume
- 294
- Issue
- 4
- Pages
- F697-F701
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2170588662
- Cited by
- 417
- References
- 46
- FWCI
- 19.92
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. https://app.cochat.ai/papers/10.1152/ajprenal.00016.2008
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- Tesch, G. H. (2008). MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy. American Journal of Physiology-Renal Physiology. https://doi.org/10.1152/ajprenal.00016.2008
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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).
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