The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Epithelial Notch signaling regulates interstitial fibrosis development in the kidneys of mice and humans
Open accessAbstract
Chronic kidney disease is a leading cause of death in the United States. Tubulointerstitial fibrosis (TIF) is considered the final common pathway leading to end-stage renal disease (ESRD). Here, we used pharmacologic, genetic, in vivo, and in vitro experiments to show that activation of the Notch pathway in tubular epithelial cells (TECs) in patients and in mouse models of TIF plays a role in TIF development. Expression of Notch in renal TECs was found to be both necessary and sufficient for TIF development. Genetic deletion of the Notch pathway in TECs reduced renal fibrosis. Consistent with this, TEC-specific expression of active Notch1 caused rapid development of TIF. Pharmacologic inhibition of Notch activation using a γ-secretase inhibitor ameliorated TIF. In summary, our experiments establish that epithelial injury and Notch signaling play key roles in fibrosis development and indicate that Notch blockade may be a therapeutic strategy to reduce fibrosis and ESRD development.
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Cites
Hypoxia requires Notch signaling to maintain the undifferentiated cell state
Gustafsson, M. V., Zheng, X., Pereira, T., Gradin, K., Jin, S., Lundkvist, J., Ruas, J. L., Poellinger, L., Lendahl, U., & Bondesson, M. (2005) · Developmental Cell · doi:10.1016/j.devcel.2005.09.010 · Cited by 1,109
Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition
Higgins, D. F., Kimura, K., Bernhardt, W. M., Shrimanker, N., Akai, Y., Hohenstein, B., Saito, Y., Johnson, R. S., Kretzler, M., Cohen, C. D., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30487 · Cited by 976
Self-citationSusztak, K., Ciccone, E., McCue, P., Sharma, K., & Böttinger, E. P. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020045 · Cited by 214
Cited by
Kang, H. M., Ahn, S. H., Choi, P., Ko, Y.-A., Han, S. H., Chinga, F., Park, A. S. D., Tao, J., Sharma, K., Pullman, J., et al. (2015) · Nature Medicine · doi:10.1038/nm.3762 · Cited by 1,555
Self-citationCellular and molecular mechanisms of renal fibrosis
Liu, Y. (2011) · Nature Reviews Nephrology · doi:10.1038/nrneph.2011.149 · Cited by 1,446
Recent Developments in Myofibroblast Biology
Hinz, B., Phan, S. H., Thannickal, V. J., Prunotto, M., Desmoulière, A., Varga, J., De Wever, O., Mareel, M., & Gabbiani, G. (2012) · The American Journal of Pathology · doi:10.1016/j.ajpath.2012.02.004 · Cited by 1,193
Single-cell transcriptomics of the mouse kidney reveals potential cellular targets of kidney disease
Park, J., Shrestha, R., Qiu, C., Kondo, A., Huang, S., Werth, M., Li, M., Barasch, J., & Suszták, K. (2018) · Science · doi:10.1126/science.aar2131 · Cited by 1,065
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
Metadata
- Authors
- Bielesz, B., Sirin, Y., Si, H., Niranjan, T., Gruenwald, A., Ahn, S., Kato, H., Pullman, J., Gessler, M., Haase, V. H., & Susztak, K.
- Venue
- Journal of Clinical Investigation
- Published
- 2010-11-01
- Volume
- 120
- Issue
- 11
- Pages
- 4040-4054
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2135032227
- Cited by
- 345
- References
- 3
- FWCI
- 14.79
- Type
- journal article
- Language
- en
- Open access
- green
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- Bielesz, B., Sirin, Y., Si, H., Niranjan, T., Gruenwald, A., Ahn, S., Kato, H., Pullman, J., Gessler, M., Haase, V. H., & Susztak, K. (2010). Epithelial Notch signaling regulates interstitial fibrosis development in the kidneys of mice and humans. Journal of Clinical Investigation. https://doi.org/10.1172/jci43025
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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.
