The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.
Fibrosis and diseases of the eye
Open accessAbstract
Most diseases that cause catastrophic loss of vision do so as a result of abnormal angiogenesis and wound healing, often in response to tissue ischemia or inflammation. Disruption of the highly ordered tissue architecture in the eye caused by vascular leakage, hemorrhage, and concomitant fibrosis can lead to mechanical disruption of the visual axis and/or biological malfunctioning. An increased understanding of inflammation, wound healing, and angiogenesis has led to the development of drugs effective in modulating these biological processes and, in certain circumstances, the preservation of vision. Unfortunately, such pharmacological interventions often are too little, too late, and progression of vision loss frequently occurs. The recent development of progenitor and/or stem cell technologies holds promise for the treatment of currently incurable ocular diseases.
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Cites
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Endostatin: an endogenous inhibitor of angiogenesis and tumor growth
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Cited by
Cellular and molecular mechanisms of fibrosis
Wynn, T. (2008) · The Journal of Pathology · doi:10.1002/path.2277 · Cited by 4,495
Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases
Wynn, T. A. (2007) · Journal of Clinical Investigation · doi:10.1172/jci31487 · Cited by 1,456
Stimulation of neural regeneration in the mouse retina
Karl, M. O., Hayes, S., Nelson, B. R., Tan, K., Buckingham, B., & Reh, T. A. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0807453105 · Cited by 368
Principles of pharmacology in the eye
Awwad, S., Mohamed Ahmed, A. H. A., Sharma, G., Heng, J. S., Khaw, P. T., Brocchini, S., & Lockwood, A. (2017) · British Journal of Pharmacology · doi:10.1111/bph.14024 · Cited by 224
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Metadata
- Authors
- Friedlander, M.
- Venue
- Journal of Clinical Investigation
- Published
- 2007-03-01
- Volume
- 117
- Issue
- 3
- Pages
- 576-586
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2142309352
- Cited by
- 299
- References
- 114
- FWCI
- 5.99
- Type
- journal article
- Language
- en
- Open access
- bronze
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Data sources
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).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
