The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Restoration of Barrier Function in Injured Intestinal Mucosa
Abstract
Mucosal repair is a complex event that immediately follows acute injury induced by ischemia and noxious luminal contents such as bile. In the small intestine, villous contraction is the initial phase of repair and is initiated by myofibroblasts that reside immediately beneath the epithelial basement membrane. Subsequent events include crawling of healthy epithelium adjacent to the wound, referred to as restitution. This is a highly regulated event involving signaling via basement membrane integrins by molecules such as focal adhesion kinase and growth factors. Interestingly, however, ex vivo studies of mammalian small intestine have revealed the importance of closure of the interepithelial tight junctions and the paracellular space. The critical role of tight junction closure is underscored by the prominent contribution of the paracellular space to measures of barrier function such as transepithelial electrical resistance. Additional roles are played by subepithelial cell populations, including neutrophils, related to their role in innate immunity. The net result of reparative mechanisms is remarkably rapid closure of mucosal wounds in mammalian tissues to prevent the onset of sepsis.
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Cites
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Tissue Destruction by Neutrophils
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Occludin: a novel integral membrane protein localizing at tight junctions.
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Resolution of inflammation: the beginning programs the end
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Decoding the Patterns of Self and Nonself by the Innate Immune System
Medzhitov, R., & Janeway, C. A. (2002) · Science · doi:10.1126/science.1068883 · Cited by 2,154
Neutrophil granules and secretory vesicles in inflammation
Faurschou, M., & Borregaard, N. (2003) · Microbes and Infection · doi:10.1016/j.micinf.2003.09.008 · Cited by 1,162
Establishment and Characterization of Cultured Epithelial Cells Lacking Expression of ZO-1
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Leaks in the epithelial barrier caused by spontaneous and TNF‐α‐induced single‐cell apoptosis
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Cited by
Intestinal barrier function: molecular regulation and disease pathogenesis
Groschwitz, K. R., & Hogan, S. P. (2009) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2009.05.038 · Cited by 1,775
Role of Ion Channels and Transporters in Cell Migration
Schwab, A., Fabian, A., Hanley, P. J., & Stock, C. (2012) · Physiological Reviews · doi:10.1152/physrev.00018.2011 · Cited by 420
DROSSMAN, D. A., CHEY, W. D., JOHANSON, J. F., FASS, R., SCOTT, C., PANAS, R., & UENO, R. (2009) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2008.03881.x · Cited by 399
Exercise-Induced Splanchnic Hypoperfusion Results in Gut Dysfunction in Healthy Men
van Wijck, K., Lenaerts, K., van Loon, L. J. C., Peters, W. H. M., Buurman, W. A., & Dejong, C. H. C. (2011) · PLoS ONE · doi:10.1371/journal.pone.0022366 · Cited by 359
“The susceptibility of the mature enterocyte population to low-flow states and ischemic events has been explained by the counter current exchange mechanism in the villus [18,19], creating a constant low oxygen environment at the villus tip.”
Backgroundvan Wijck, K., Lenaerts, K., Grootjans, J., Wijnands, K. A. P., Poeze, M., van Loon, L. J. C., Dejong, C. H. C., & Buurman, W. A. (2012) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00066.2012 · Cited by 285
Metadata
- Authors
- Blikslager, A. T., Moeser, A. J., Gookin, J. L., Jones, S. L., & Odle, J.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2007-04
- Volume
- 87
- Issue
- 2
- Pages
- 545-564
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2018815492
- Cited by
- 574
- References
- 9
- FWCI
- 3.97
- Type
- journal article
- Language
- en
- Open access
- closed
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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.
