The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Endothelial to Mesenchymal Transition (EndoMT) in the Pathogenesis of Human Fibrotic Diseases
Open accessAbstract
Fibrotic diseases encompass a wide spectrum of clinical entities including systemic fibrotic diseases such as systemic sclerosis, sclerodermatous graft versus host disease, nephrogenic systemic fibrosis, and IgG4-associated sclerosing disease, as well as numerous organ-specific disorders including radiation-induced fibrosis, and cardiac, pulmonary, liver, and kidney fibrosis. Although their causative mechanisms are quite diverse, these diseases share the common feature of an uncontrolled and progressive accumulation of fibrous tissue macromolecules in affected organs leading to their dysfunction and ultimate failure. The pathogenesis of fibrotic diseases is complex and despite extensive investigation has remained elusive. Numerous studies have identified myofibroblasts as the cells responsible for the establishment and progression of the fibrotic process. Tissue myofibroblasts in fibrotic diseases originate from several sources including quiescent tissue fibroblasts, circulating CD34+ fibrocytes, and the phenotypic conversion of various cell types including epithelial and endothelial cells into activated myofibroblasts. However, the role of the phenotypic transition of endothelial cells into mesenchymal cells (Endothelial to Mesenchymal Transition or EndoMT) in the pathogenesis of fibrotic disorders has not been fully elucidated. Here, we review the evidence supporting EndoMT’s contribution to human fibrotic disease pathogenesis.
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Cites
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Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition
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“These studies have shown that myofibroblasts can originate from various sources including expansion and activation of quiescent resident tissue fibroblasts [42], migration and tissue accumulation of bone marrow-derived CD34+ fibrocytes [43,44], or from the phenotypic transition of epithelial cells, a process known as…”
NADPH oxidase-4 mediates myofibroblast activation and fibrogenic responses to lung injury
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Cited by
Endothelial to Mesenchymal Transition in Cardiovascular Disease
Kovacic, J. C., Dimmeler, S., Harvey, R. P., Finkel, T., Aikawa, E., Krenning, G., & Baker, A. H. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.09.089 · Cited by 631
Organ and tissue fibrosis: Molecular signals, cellular mechanisms and translational implications
Weiskirchen, R., Weiskirchen, S., & Tacke, F. (2019) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2018.06.003 · Cited by 538
Pathophysiology of systemic sclerosis: current understanding and new insights
Cutolo, M., Soldano, S., & Smith, V. (2019) · Expert Review of Clinical Immunology · doi:10.1080/1744666x.2019.1614915 · Cited by 369
Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease
Hammoutene, A., & Rautou, P.-E. (2019) · Journal of Hepatology · doi:10.1016/j.jhep.2019.02.012 · Cited by 364
Varga, J., Trojanowska, M., & Kuwana, M. (2017) · Journal of Scleroderma and Related Disorders · doi:10.5301/jsrd.5000249 · Cited by 323
Metadata
- Authors
- Piera-Velazquez, S., Mendoza, F., & Jimenez, S.
- Venue
- Journal of Clinical Medicine
- Publisher
- MDPI AG
- Published
- 2016-04-11
- Volume
- 5
- Issue
- 4
- Pages
- 45
- ISSN
- 2077-0383 (ISSN-L)
- OpenAlex
- W2332128473
- Cited by
- 273
- References
- 18
- FWCI
- 28.92
- Type
- journal article
- Language
- en
- Open access
- gold
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- Piera-Velazquez, S., Mendoza, F., & Jimenez, S. (2016). Endothelial to Mesenchymal Transition (EndoMT) in the Pathogenesis of Human Fibrotic Diseases. Journal of Clinical Medicine. https://doi.org/10.3390/jcm5040045
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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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