Živanović Nemanja, Lesjak Marija, Simin Nataša, Srai Surjit K S
Department of Chemistry, Biochemistry and Environmental Protection, Faculty of Sciences, University of Novi Sad, Trg Dositeja Obradovica 3, 21000 Novi Sad, Serbia.
Research Department of Structural and Molecular Biology, Division of Biosciences, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK.
Antioxidants (Basel). 2024 Mar 10;13(3):334. doi: 10.3390/antiox13030334.
Ferroptosis is a recently discovered type of programmed cell death that is mechanistically different from other types of programmed cell death such as apoptosis, necroptosis, and autophagy. It is characterized by the accumulation of intracellular iron, overproduction of reactive oxygen species, depletion of glutathione, and extensive lipid peroxidation of lipids in the cell membrane. It was discovered that ferroptosis is interconnected with many diseases, such as neurodegenerative diseases, ischemia/reperfusion injury, cancer, and chronic kidney disease. Polyphenols, plant secondary metabolites known for many bioactivities, are being extensively researched in the context of their influence on ferroptosis which resulted in a great number of publications showing the need for a systematic review. In this review, an extensive literature search was performed. Databases (Scopus, Web of Science, PubMed, ScienceDirect, Springer) were searched in the time span from 2017 to November 2023, using the keyword "ferroptosis" alone and in combination with "flavonoid", "phenolic acid", "stilbene", "coumarin", "anthraquinone", and "chalcone"; after the selection of studies, we had 311 papers and 143 phenolic compounds. In total, 53 compounds showed the ability to induce ferroptosis, and 110 compounds were able to inhibit ferroptosis, and out of those compounds, 20 showed both abilities depending on the model system. The most researched compounds are shikonin, curcumin, quercetin, resveratrol, and baicalin. The most common modes of action are in the modulation of the Nrf2/GPX4 and Nrf2/HO-1 axis and the modulation of iron metabolism.
铁死亡是一种最近发现的程序性细胞死亡类型，其机制与其他类型的程序性细胞死亡如凋亡、坏死性凋亡和自噬不同。它的特征是细胞内铁的积累、活性氧的过度产生、谷胱甘肽的消耗以及细胞膜脂质的广泛过氧化。人们发现铁死亡与许多疾病相互关联，如神经退行性疾病、缺血/再灌注损伤、癌症和慢性肾病。多酚是具有多种生物活性的植物次生代谢产物，目前正在广泛研究它们对铁死亡的影响，这导致大量出版物表明有必要进行系统综述。在本综述中，进行了广泛的文献检索。在2017年至2023年11月的时间跨度内，使用关键词“铁死亡”单独以及与“黄酮类化合物”、“酚酸”、“芪类”、“香豆素”、“蒽醌”和“查耳酮”组合检索数据库（Scopus、科学网、PubMed、ScienceDirect、Springer）；在筛选研究后，我们得到了311篇论文和143种酚类化合物。总共有53种化合物显示出诱导铁死亡的能力，110种化合物能够抑制铁死亡，在这些化合物中，有20种根据模型系统显示出两种能力。研究最多的化合物是紫草素、姜黄素、槲皮素、白藜芦醇和黄芩苷。最常见的作用方式是调节Nrf2/GPX4和Nrf2/HO-1轴以及调节铁代谢。
