The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
Degradative Action of Reactive Oxygen Species on Hyaluronan
Abstract
Many human diseases are associated with harmful action of reactive oxygen species (ROS). These species are involved in the degradation of essential tissue or related components. One of such components is synovial fluid that contains a high-molecular-weight polymer--hyaluronan (HA). Uninhibited and/or inhibited hyaluronan degradation by the action of various ROS has been studied in many in vitro models. In these studies, the change of the molecular weight of HA or a related parameter, such as HA solution viscosity, has been used as a marker of inflicted damage. The aim of the presented review is to briefly summarize the available data. Their correct interpretation could contribute to the implementation of modern methods of evaluation of the antioxidative capacity of natural and synthetic substances and prospective drugs--potential inflammatory disease modifying agents. Another focus of this review is to evaluate briefly the impact of different available analytical techniques currently used to investigate the structure of native high-molecular-weight hyaluronan and/or of its fragments.
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Cites
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Cited by
Hyaluronan as an Immune Regulator in Human Diseases
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Therapeutic strategies for enhancing angiogenesis in wound healing
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Proteoglycan Chemical Diversity Drives Multifunctional Cell Regulation and Therapeutics
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Metadata
- Authors
- Šoltés, L., Mendichi, R., Kogan, G., Schiller, J., Stankovská, M., & Arnhold, J.
- Venue
- Biomacromolecules
- Publisher
- American Chemical Society (ACS)
- Published
- 2006-02-16
- Volume
- 7
- Issue
- 3
- Pages
- 659-668
- ISSN
- 1525-7797 (ISSN-L)
- 1526-4602
- OpenAlex
- W2036672354
- Cited by
- 329
- References
- 53
- FWCI
- 4.49
- 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).
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