The DOI matches its Crossref record; 105 of the 105 references it cites were found in a registry or an index.
Fibroblasts in myocardial infarction: A role in inflammation and repair
Open accessAbstract
Fibroblasts do not only serve as matrix-producing reparative cells, but exhibit a wide range of functions in inflammatory and immune responses, angiogenesis and neoplasia. The adult mammalian myocardium contains abundant fibroblasts enmeshed within the interstitial and perivascular extracellular matrix. The current review manuscript discusses the dynamic phenotypic and functional alterations of cardiac fibroblasts following myocardial infarction. Extensive necrosis of cardiomyocytes in the infarcted heart triggers an intense inflammatory reaction. In the early stages of infarct healing, fibroblasts become pro-inflammatory cells, activating the inflammasome and producing cytokines, chemokines and proteases. Pro-inflammatory cytokines (such as Interleukin-1) delay myofibroblast transformation, until the wound is cleared from dead cells and matrix debris. Resolution of the inflammatory infiltrate is associated with fibroblast migration, proliferation, matrix protein synthesis and myofibroblast conversion. Growth factors and matricellular proteins play an important role in myofibroblast activation during the proliferative phase of healing. Formation of a mature cross-linked scar is associated with clearance of fibroblasts, as poorly-understood inhibitory signals restrain the fibrotic response. However, in the non-infarcted remodeling myocardium, local fibroblasts may remain activated in response to volume and pressure overload and may promote interstitial fibrosis. Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling.
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Cites
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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis
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Formation and function of the myofibroblast during tissue repair
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Fate Tracing Reveals the Pericyte and Not Epithelial Origin of Myofibroblasts in Kidney Fibrosis
Humphreys, B. D., Lin, S.-L., Kobayashi, A., Hudson, T. E., Nowlin, B. T., Bonventre, J. V., Valerius, M. T., McMahon, A. P., & Duffield, J. S. (2010) · The American Journal of Pathology · doi:10.2353/ajpath.2010.090517 · Cited by 1,442
TGF-ß Signaling in Fibroblasts Modulates the Oncogenic Potential of Adjacent Epithelia
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Self-citationCardiac Fibroblast: The Renaissance Cell
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Transforming growth factor (TGF)-β signaling in cardiac remodeling
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Self-citationStructural and functional characterisation of cardiac fibroblasts
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Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer
Wu, F., Yang, J., Liu, J., Wang, Y., Mu, J., Zeng, Q., Deng, S., & Zhou, H. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00641-0 · Cited by 773
Spatial multi-omic map of human myocardial infarction
Kuppe, C., Ramirez Flores, R. O., Li, Z., Hayat, S., Levinson, R. T., Liao, X., Hannani, M. T., Tanevski, J., Wünnemann, F., Nagai, J. S., et al. (2022) · Nature · doi:10.1038/s41586-022-05060-x · Cited by 772
Redefining the identity of cardiac fibroblasts
Tallquist, M. D., & Molkentin, J. D. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2017.57 · Cited by 581
Russo, I., & Frangogiannis, N. G. (2016) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.12.011 · Cited by 474
Self-citationMechanical regulation of myofibroblast phenoconversion and collagen contraction
Hinz, B., McCulloch, C. A., & Coelho, N. M. (2019) · Experimental Cell Research · doi:10.1016/j.yexcr.2019.03.027 · Cited by 182
Metadata
- Authors
- Shinde, A. V., & Frangogiannis, N. G.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 70
- Pages
- 74-82
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2051521659
- Cited by
- 522
- References
- 105
- FWCI
- 18.43
- Type
- journal article
- Language
- en
- Open access
- green
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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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