The role of the ferroptosis pathway in the regulation of polysaccharides for human health: A review
Polysaccharides are natural polymers with ketone or aldehyde groups that are widely found in plants, animals, and microorganisms. They exhibit various biological activities and have potential development value in the food and pharmaceutical fields. Ferroptosis is a recently discovered modality that...
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Veröffentlicht in: | International journal of biological macromolecules 2023-03, Vol.231, p.123349-123349, Article 123349 |
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Sprache: | eng |
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Zusammenfassung: | Polysaccharides are natural polymers with ketone or aldehyde groups that are widely found in plants, animals, and microorganisms. They exhibit various biological activities and have potential development value in the food and pharmaceutical fields. Ferroptosis is a recently discovered modality that modulates cell death and has attracted considerable attention because it is considered to be involved in many pathophysiological processes. The inhibition of ferroptosis by reducing intracellular iron accumulation and lipid peroxidation may provide potential protective strategies against related pathologies. Ferroptosis is also involved in the physiological activities of polysaccharides, and its regulatory mechanism varies according to different physiological activities. However, a systematic summary on the involvement of ferroptosis in the physiological activities of polysaccharides is currently lacking. Therefore, this review systematically summarized the relationship between the physiological activities of polysaccharides and ferroptosis and focused on the regulatory mechanism of ferroptosis, with respect to the anti-cancer, anti-inflammatory, antioxidant, and immunomodulatory activities of all polysaccharides. The primary objective was to find new polysaccharide-related therapeutic breakthroughs for related diseases and to provide a reference for further research on polysaccharides-based therapeutics.
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ISSN: | 0141-8130 1879-0003 |
DOI: | 10.1016/j.ijbiomac.2023.123349 |