The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Myofibroblast differentiation and survival in fibrotic disease
Open accessAbstract
During wound healing, contractile fibroblasts called myofibroblasts regulate the formation and contraction of granulation tissue; however, pathological and persistent myofibroblast activation, which occurs in hypertrophic scars or tissue fibrosis, results in a loss of function. Many reviews outline the cellular and molecular features of myofibroblasts and their roles in a variety of diseases. This review focuses on the origins of myofibroblasts and the factors that control their differentiation and prolonged survival in fibrotic tissues. Pulmonary fibrosis is used to illustrate many key points, but examples from other tissues and models are also included. Myofibroblasts originate mostly from tissue-resident fibroblasts, and also from epithelial and endothelial cells or other mesenchymal precursors. Their differentiation is influenced by cytokines, growth factors, extracellular matrix composition and stiffness, and cell surface molecules such as proteoglycans and THY1, among other factors. Many of these effects are modulated by cell contraction. Myofibroblasts resist programmed cell death, which promotes their accumulation in fibrotic tissues. The cause of resistance to apoptosis in myofibroblasts is under ongoing investigation, but many of the same stimuli that regulate their differentiation are involved. The contributions of oxidative stress, the WNT–β-catenin pathway and PPARγ to myofibroblast differentiation and survival are increasingly appreciated.
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Cites
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Formation and function of the myofibroblast during tissue repair
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Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix
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Cited by
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
Genetic lineage tracing defines myofibroblast origin and function in the injured heart
Kanisicak, O., Khalil, H., Ivey, M. J., Karch, J., Maliken, B. D., Correll, R. N., Brody, M. J., J. Lin, S.-C., Aronow, B. J., Tallquist, M. D., et al. (2016) · Nature Communications · doi:10.1038/ncomms12260 · Cited by 892
The myofibroblast matrix: implications for tissue repair and fibrosis
Klingberg, F., Hinz, B., & White, E. S. (2013) · The Journal of Pathology · doi:10.1002/path.4104 · Cited by 776
Glycolytic Reprogramming in Myofibroblast Differentiation and Lung Fibrosis
Xie, N., Tan, Z., Banerjee, S., Cui, H., Ge, J., Liu, R.-M., Bernard, K., Thannickal, V. J., & Liu, G. (2015) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201504-0780oc · Cited by 582
TGF‐β as a driver of fibrosis: physiological roles and therapeutic opportunities
Budi, E. H., Schaub, J. R., Decaris, M., Turner, S., & Derynck, R. (2021) · The Journal of Pathology · doi:10.1002/path.5680 · Cited by 292
Metadata
- Authors
- Kis, K., Liu, X., & Hagood, J. S.
- Venue
- Expert Reviews in Molecular Medicine
- Publisher
- Cambridge University Press (CUP)
- Published
- 2011-08
- Volume
- 13
- Pages
- e27-e27
- ISSN
- 1462-3994 (ISSN-L)
- OpenAlex
- W2016613783
- Cited by
- 224
- References
- 23
- FWCI
- 10.64
- Type
- journal article
- Language
- en
- Open access
- green
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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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