The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Macrophages in streptozotocin-induced diabetic nephropathy: potential role in renal fibrosis
Abstract
BACKGROUND: Renal fibrosis is central to the progression of diabetic nephropathy; however, the mechanisms responsible for fibroblast and matrix accumulation in this disease are only partially understood. Macrophages accumulate in diabetic kidneys, but it is unknown whether macrophages contribute to renal fibrosis. Therefore, we examined whether macrophage accumulation is associated with the progression of renal injury and fibrosis in type 1 diabetic nephropathy and whether macrophages exposed to the diabetic milieu could promote fibroblast proliferation. METHODS: Kidney macrophages, renal injury and fibrosis were analysed in diabetic C57BL/6J mice at 2, 8, 12 and 18 weeks after streptozotocin injection. Isolated rat bone marrow macrophages were stimulated with diabetic rat serum or carboxymethyllysine (CML)-bovine serum albumin (BSA) to determine whether macrophage-conditioned medium could promote the proliferation of rat renal (NRK-49F) fibroblasts. RESULTS: Progressive injury and fibrosis in diabetic nephropathy was associated with increased numbers of kidney macrophages. Macrophage accumulation in diabetic mice correlated with hyperglycaemia (blood glucose, HbA1c levels), renal injury (albuminuria, plasma creatinine), histological damage and renal fibrosis (myofibroblasts, collagen IV). Culture supernatant derived from bone marrow macrophages incubated with diabetic rat serum or CML-BSA induced proliferation of fibroblasts, which was inhibited by pre-treating fibroblasts with interleukin-1 (IL-1) receptor antagonist or the platelet-derived growth factor (PDGF) receptor kinase inhibitor, STI-571. CONCLUSION: Kidney macrophage accumulation is associated with the progression of renal injury and fibrosis in streptozotocin-induced mouse diabetic nephropathy. Elements of the diabetic milieu can stimulate macrophages to promote fibroblast proliferation via IL-1- and PDGF-dependent pathways which may enhance renal fibrosis.
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Citations
Cites
Role of Advanced Glycation End Products in Diabetic Nephropathy
Forbes, J. M., Cooper, M. E., Oldfield, M. D., & Thomas, M. C. (2003) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000077413.41276.17 · Cited by 351
Cited by
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
Tesch, G. H. (2008) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00016.2008 · Cited by 417
Self-citationDiabetic nephropathy – is this an immune disorder?
Tesch, G. H. (2017) · Clinical Science · doi:10.1042/cs20160636 · Cited by 264
Self-citationImmune responses in diabetic nephropathy: Pathogenic mechanisms and therapeutic target
Chen, J., Liu, Q., He, J., & Li, Y. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.958790 · Cited by 164
Zhu, X., Cheng, Y.-Q., Du, L., Li, Y., Zhang, F., Guo, H., Liu, Y.-W., & Yin, X.-X. (2015) · Phytotherapy Research · doi:10.1002/ptr.5254 · Cited by 66
Metadata
- Authors
- Chow, F. Y., Nikolic-Paterson, D. J., Atkins, R. C., & Tesch, G. H.
- Venue
- Nephrology Dialysis Transplantation
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-12-01
- Volume
- 19
- Issue
- 12
- Pages
- 2987-2996
- ISSN
- 0931-0509 (ISSN-L)
- 1460-2385
- OpenAlex
- W2103813608
- Cited by
- 206
- References
- 1
- FWCI
- 3.06
- Type
- journal article
- Language
- en
- Open access
- closed
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- Chow, F. Y., Nikolic-Paterson, D. J., Atkins, R. C., & Tesch, G. H. (2004). Macrophages in streptozotocin-induced diabetic nephropathy: potential role in renal fibrosis. Nephrology Dialysis Transplantation. https://doi.org/10.1093/ndt/gfh441
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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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