Université de Lorraine, CITHEFOR, F-54505 Vandoeuvre Les Nancy, France.
Université de Lorraine, CNRS, LRGP, F-54000 Nancy, France.
Molecules. 2023 Mar 14;28(6):2636. doi: 10.3390/molecules28062636.
Ferroptosis is a type of cell death driven by iron overload and lipid peroxidation. It is considered a key mechanism in the development of various diseases such as atherosclerosis, Alzheimer, diabetes, cancer, and renal failure. The redox status of cells, such as the balance between intracellular oxidants (lipid peroxides, reactive oxygen species, free iron ions) and antioxidants (glutathione, glutathione Peroxidase 4), plays a major role in ferroptosis regulation and constitutes its principal biomarkers. Therefore, the induction and inhibition of ferroptosis are promising strategies for disease treatments such as cancer or neurodegenerative and cardiovascular diseases, respectively. Many drugs have been developed to exert ferroptosis-inducing and/or inhibiting reactions, such as erastin and iron-chelating compounds, respectively. In addition, many natural bioactive compounds have significantly contributed to regulating ferroptosis and ferroptosis-induced oxidative stress. Natural bioactive compounds are largely abundant in food and plants and have been for a long time, inspiring the development of various low-toxic therapeutic drugs. Currently, functional bioactive peptides are widely reported for their antioxidant properties and application in human disease treatment. The scientific evidence from biochemical and in vitro tests of these peptides strongly supports the existence of a relationship between their antioxidant properties (such as iron chelation) and ferroptosis regulation. In this review, we answer questions concerning ferroptosis milestones, its importance in physiopathology mechanisms, and its downstream regulatory mechanisms. We also address ferroptosis regulatory natural compounds as well as provide promising thoughts about bioactive peptides.
铁死亡是一种由铁过载和脂质过氧化驱动的细胞死亡方式。它被认为是动脉粥样硬化、阿尔茨海默病、糖尿病、癌症和肾衰竭等多种疾病发展的关键机制。细胞的氧化还原状态,如细胞内氧化剂(脂质过氧化物、活性氧物种、游离铁离子)和抗氧化剂(谷胱甘肽、谷胱甘肽过氧化物酶 4)之间的平衡,在铁死亡调节中起着重要作用,并构成其主要生物标志物。因此,诱导和抑制铁死亡分别是癌症或神经退行性和心血管疾病等疾病治疗的有前途的策略。已经开发了许多药物来发挥铁死亡诱导和/或抑制反应,例如分别为 erastin 和铁螯合剂。此外,许多天然生物活性化合物在调节铁死亡和铁死亡诱导的氧化应激方面做出了重大贡献。天然生物活性化合物在很大程度上丰富于食物和植物中,并且长期以来一直激发着各种低毒治疗药物的开发。目前,功能性生物活性肽因其抗氧化特性及其在人类疾病治疗中的应用而被广泛报道。这些肽的生化和体外测试的科学证据强烈支持它们的抗氧化特性(如铁螯合)与铁死亡调节之间存在关系。在这篇综述中,我们回答了有关铁死亡里程碑、其在生理病理学机制中的重要性以及其下游调节机制的问题。我们还讨论了铁死亡调节天然化合物,并提供了关于生物活性肽的有前途的思路。