The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy.
Open accessAbstract
Diabetes is now the most common cause of progressive kidney failure leading to dialysis or transplantation. The central pathological feature of diabetic nephropathy is accumulation of extracellular matrix within the glomeruli. The factors in the diabetic milieu responsible for extracellular matrix accumulation are not understood. Here we report that in glomeruli of rats made diabetic there is a slow, progressive increase in the expression of transforming growth factor beta (TGF-beta) mRNA and TGF-beta protein. A key action of TGF-beta is induction of extracellular matrix production, and specific matrix proteins known to be induced by TGF-beta were increased in diabetic rat glomeruli. These proteins include an alternatively spliced form of fibronectin, tenascin, and the proteoglycan biglycan. TGF-beta has not previously been implicated in the matrix accumulation that occurs in the diabetic kidney. Glomeruli from humans with diabetic nephropathy also showed a striking increase in immunoreactive TGF-beta protein and deposition of the special form of fibronectin, whereas glomeruli from normal subjects or from individuals with other glomerular diseases (where extracellular matrix accumulation is not a feature) were negative or barely positive. These results implicate TGF-beta in the pathogenesis of diabetic nephropathy.
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Cites
Ignotz, R. A., & Massagué, J. (1986) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)35666-1 · Cited by 2,492
Stimulation of the chemotactic migration of human fibroblasts by transforming growth factor beta.
Postlethwaite, A. E., Keski-Oja, J., Moses, H. L., & Kang, A. H. (1987) · The Journal of experimental medicine · doi:10.1084/jem.165.1.251 · Cited by 777
Induction of tenascin in healing wounds
Mackie, E. J., Halfter, W., & Liverani, D. (1988) · The Journal of cell biology · doi:10.1083/jcb.107.6.2757 · Cited by 555
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Self-citationCell adhesion protein receptors as targets for transforming growth factor-$beta; action
IGNOTZ, R. (1987) · Cell · doi:10.1016/0092-8674(87)90146-2 · Cited by 485
Cited by
TGF-β: the master regulator of fibrosis
Meng, X.-M., Nikolic-Paterson, D. J., & Lan, H. Y. (2016) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.48 · Cited by 3,528
Activation of latent TGF-β by thrombospondin-1: mechanisms and physiology
Murphy-Ullrich, J. E., & Poczatek, M. (2000) · Cytokine & Growth Factor Reviews · doi:10.1016/s1359-6101(99)00029-5 · Cited by 586
TGF-β activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN
Kato, M., Putta, S., Wang, M., Yuan, H., Lanting, L., Nair, I., Gunn, A., Nakagawa, Y., Shimano, H., Todorov, I., et al. (2009) · Nature Cell Biology · doi:10.1038/ncb1897 · Cited by 573
mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice
Inoki, K., Mori, H., Wang, J., Suzuki, T., Hong, S., Yoshida, S., Blattner, S. M., Ikenoue, T., Rüegg, M. A., Hall, M. N., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44771 · Cited by 538
Therapeutic Potential of Nrf2 Activators in Streptozotocin-Induced Diabetic Nephropathy
Zheng, H., Whitman, S. A., Wu, W., Wondrak, G. T., Wong, P. K., Fang, D., & Zhang, D. D. (2011) · Diabetes · doi:10.2337/db11-0807 · Cited by 507
Metadata
- Authors
- Yamamoto, T., Nakamura, T., Noble, N. A., Ruoslahti, E., & Border, W. A.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1993-03
- Volume
- 90
- Issue
- 5
- Pages
- 1814-1818
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2091321868
- Cited by
- 830
- References
- 5
- FWCI
- 29.79
- Type
- journal article
- Language
- en
- Open access
- green
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- Yamamoto, T., Nakamura, T., Noble, N. A., Ruoslahti, E., & Border, W. A. (1993). Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.90.5.1814
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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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