The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Resident fibroblast lineages mediate pressure overload–induced cardiac fibrosis
Open accessAbstract
Activation and accumulation of cardiac fibroblasts, which result in excessive extracellular matrix deposition and consequent mechanical stiffness, myocyte uncoupling, and ischemia, are key contributors to heart failure progression. Recently, endothelial-to-mesenchymal transition (EndoMT) and the recruitment of circulating hematopoietic progenitors to the heart have been reported to generate substantial numbers of cardiac fibroblasts in response to pressure overload-induced injury; therefore, these processes are widely considered to be promising therapeutic targets. Here, using multiple independent murine Cre lines and a collagen1a1-GFP fusion reporter, which specifically labels fibroblasts, we found that following pressure overload, fibroblasts were not derived from hematopoietic cells, EndoMT, or epicardial epithelial-to-mesenchymal transition. Instead, pressure overload promoted comparable proliferation and activation of two resident fibroblast lineages, including a previously described epicardial population and a population of endothelial origin. Together, these data present a paradigm for the origins of cardiac fibroblasts during development and in fibrosis. Furthermore, these data indicate that therapeutic strategies for reducing pathogenic cardiac fibroblasts should shift from targeting presumptive EndoMT or infiltrating hematopoietically derived fibroblasts, toward common pathways upregulated in two endogenous fibroblast populations.
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1 retracted
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RetractedCluster analysis and display of genome-wide expression patterns
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Cited by
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
Revisiting Cardiac Cellular Composition
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“The use of CD90 for identification of fibroblasts, on the contrary, remains a point of debate.(17,35) Previously, we have shown that cardiac Tcf21 lineage cells, and GFP cells from PDGFRα and Col1a1-GFP mouse hearts have similar levels of fibroblast gene expression including Col3a1, Col6a1, Dcn, and MMP2 with lack of…”
BackgroundFibrosis–a common pathway to organ injury and failure
Rockey, D. C., Bell, P. D., & Hill, J. A. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1300575 · Cited by 1,428
CAR T cells produced in vivo to treat cardiac injury
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Frangogiannis, N. G. (2021) · Cardiovascular Research · doi:10.1093/cvr/cvaa324 · Cited by 1,229
Metadata
- Authors
- Moore-Morris, T., Guimarães-Camboa, N., Banerjee, I., Zambon, A. C., Kisseleva, T., Velayoudon, A., Stallcup, W. B., Gu, Y., Dalton, N. D., Cedenilla, M., Gomez-Amaro, R., Zhou, B., Brenner, D. A., Peterson, K. L., Chen, J., & Evans, S. M.
- Venue
- Journal of Clinical Investigation
- Published
- 2014-06-17
- Volume
- 124
- Issue
- 7
- Pages
- 2921-2934
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1974848384
- Cited by
- 630
- References
- 52
- FWCI
- 34.96
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Moore-Morris, T., Guimarães-Camboa, N., Banerjee, I., Zambon, A. C., Kisseleva, T., Velayoudon, A., Stallcup, W. B., Gu, Y., Dalton, N. D., Cedenilla, M., Gomez-Amaro, R., Zhou, B., Brenner, D. A., Peterson, K. L., Chen, J., & Evans, S. M. (2014). Resident fibroblast lineages mediate pressure overload–induced cardiac fibrosis. Journal of Clinical Investigation. https://doi.org/10.1172/jci74783
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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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