The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice
Open accessAbstract
Cardiac fibrosis is characterized by excessive extracellular matrix deposition that contributes to compromised cardiac function and potentially heart failure. Cardiac pressure overload resulting from trans-aortic constriction in mice leads to cardiac fibrosis and increased Wnt/β-catenin signaling in cardiac fibroblasts. Here, we conditionally induce β-catenin loss of function in resident cardiac fibroblasts using Tcf21 MerCreMer or in activated cardiac fibroblasts using periostin (Postn) MerCreMer . We show that β-catenin loss of function in cardiac fibroblasts after trans-aortic constriction significantly preserves cardiac function, and reduces interstitial fibrosis but does not alter the numbers of activated or differentiated cardiac fibroblasts in vivo. However, β-catenin is specifically required in resident cardiac fibroblasts for fibrotic excessive extracellular matrix gene expression and binds Col3a1 and Postn gene sequences in cultured cardiac fibroblasts after induction of Wnt signaling. Moreover, cardiomyocyte hypertrophy is blunted with cardiac fibroblast-specific loss of β-catenin after trans-aortic constriction in vivo. Thus, Wnt/β-catenin signaling in resident cardiac fibroblasts is required for excessive extracellular matrix gene expression and collagen deposition after trans-aortic constriction.
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Cites
Cardiac Fibrosis: The Fibroblast Awakens
Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C. (2016) · Circulation Research · doi:10.1161/circresaha.115.306565 · Cited by 1,596
Self-citationRevisiting Cardiac Cellular Composition
Pinto, A. R., Ilinykh, A., Ivey, M. J., Kuwabara, J. T., D’Antoni, M. L., Debuque, R., Chandran, A., Wang, L., Arora, K., Rosenthal, N. A., et al. (2016) · Circulation Research · doi:10.1161/circresaha.115.307778 · Cited by 1,400
Activation of canonical Wnt signalling is required for TGF-β-mediated fibrosis
Akhmetshina, A., Palumbo, K., Dees, C., Bergmann, C., Venalis, P., Zerr, P., Horn, A., Kireva, T., Beyer, C., Zwerina, J., et al. (2012) · Nature Communications · doi:10.1038/ncomms1734 · Cited by 843
Acharya, A., Baek, S. T., Huang, G., Eskiocak, B., Goetsch, S., Sung, C. Y., Banfi, S., Sauer, M. F., Olsen, G. S., Duffield, J. S., et al. (2012) · Development · doi:10.1242/dev.079970 · Cited by 498
Cardiac hypertrophy is not a required compensatory response to short-term pressure overload
Hill, J. A., Karimi, M., Kutschke, W., Davisson, R. L., Zimmerman, K., Wang, Z., Kerber, R. E., & Weiss, R. M. (2000) · Circulation · doi:10.1161/01.cir.101.24.2863 · Cited by 309
β-catenin is a central mediator of pro-fibrotic Wnt signaling in systemic sclerosis
Beyer, C., Schramm, A., Akhmetshina, A., Dees, C., Kireva, T., Gelse, K., Sonnylal, S., de Crombrugghe, B., Taketo, M. M., Distler, O., et al. (2012) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2011-200568 · Cited by 203
Cell-cell interaction in the heart via Wnt/ -catenin pathway after cardiac injury
Deb, A. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu054 · Cited by 102
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Zhang, Q., Wang, L., Wang, S., Cheng, H., Xu, L., Pei, G., Wang, Y., Fu, C., Jiang, Y., He, C., et al. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-00925-z · Cited by 831
Cellular mechanotransduction in health and diseases: from molecular mechanism to therapeutic targets
Di, X., Gao, X., Peng, L., Ai, J., Jin, X., Qi, S., Li, H., Wang, K., & Luo, D. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01501-9 · Cited by 622
Single-Cell Deconvolution of Fibroblast Heterogeneity in Mouse Pulmonary Fibrosis
Xie, T., Wang, Y., Deng, N., Huang, G., Taghavifar, F., Geng, Y., Liu, N., Kulur, V., Yao, C., Chen, P., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.03.010 · Cited by 527
Metadata
- Authors
- Xiang, F.-L., Fang, M., & Yutzey, K. E.
- Venue
- Nature Communications
- Published
- 2017-09-28
- Volume
- 8
- Issue
- 1
- Pages
- 712-712
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2758667350
- Cited by
- 201
- References
- 7
- FWCI
- 11.60
- Type
- journal article
- Language
- en
- Open access
- gold
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- Xiang, F.-L., Fang, M., & Yutzey, K. E. (2017). Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice. Nature Communications. https://doi.org/10.1038/s41467-017-00840-w
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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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