The DOI matches its Crossref record; 108 of the 108 references it cites were found in a registry or an index.
Novel advances in inhibiting advanced glycation end product formation using natural compounds
Open accessAbstract
Advanced glycation end products (AGEs) are a group of complex compounds generated by nonenzymatic interactions between proteins and reducing sugars or lipids. AGEs accumulate in vivo and activate various signaling pathways closely related to the occurrence of various chronic metabolic diseases. In this paper, we describe the process through which AGEs are formed, the classification of AGEs, and biological effects of AGEs on human health. Most importantly, we review recent progress in natural compound-based AGE formation inhibitors. Major classes of natural inhibitors, including polyphenols, polysaccharides, terpenoids, vitamins and alkaloids, have been described. Their mechanisms of action have been summarized as scavenging free radicals, chelating metal ions, capturing active carbonyl compounds, protecting protein glycation sites, and lowering blood glucose levels. Although these natural compounds have good antiglycation activity, to date, they are not widely used in the clinic, likely because of their low content levels. However, these natural compounds and their molecular frameworks will play a valuable role in inspiring drug discovery.
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Cites
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Advanced glycation endproducts in food and their effects on health
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Iron-chelation properties of phenolic acids bearing catechol and galloyl groups
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Metadata
- Authors
- Song, Q., Liu, J., Dong, L., Wang, X., & Zhang, X.
- Venue
- Biomedicine & Pharmacotherapy
- Publisher
- Elsevier BV
- Published
- 2021-08
- Volume
- 140
- Pages
- 111750
- ISSN
- 0753-3322 (ISSN-L)
- OpenAlex
- W3165480716
- Cited by
- 257
- References
- 108
- FWCI
- 21.53
- Type
- journal article
- Language
- en
- Open access
- gold
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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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