Lather Simran, Garg Neera
Department of Botany, Panjab University, Chandigarh, 160014, India.
Plant Physiol Biochem. 2025 Jul 8;228:110221. doi: 10.1016/j.plaphy.2025.110221.
Ferroptosis, a recently discovered cell death mechanism, is distinguished from other forms of regulated cell death by the iron-controlled build-up of lipid reactive oxygen species (ROS). Originally illustrated in animals, ferroptosis has eventually been discovered in plant cells conferring multiple hallmarks with animal systems. This cell death pathway in plants is associated with iron homeostasis mechanisms, which are vital for regulating the dual nature of iron as both essential and potentially toxic. The critical elements connected with ferroptosis in plants comprise of lipid metabolism enzymes, iron chelators, ROS scavenging systems and exhaustion of glutathione as well as ascorbic acid. Cell death due to ferroptosis is assisted by the generation of lipid peroxides and mitochondrial shrinkage. However, application of inhibitors of ferroptosis, including ferrostatin-1 and ciclopirox olamine, can hinder cell damage by inhibiting the build-up of lipid peroxides and ROS. Moreover, in order to modulate plant ferroptosis, signaling pathways as well as transcription factors sensitive to oxidative burden and iron are also crucial. Ferroptosis in plants is a complex pathway and consists of various compartments at cellular level, such as chloroplasts, mitochondria and cytosol. The distinctiveness of plant systems due to their definite metabolic mechanisms and significant degree of compartmentalization further affix intricacies to the trajectory of ferroptosis. Therefore, this review delves into the current understanding of ferroptosis in plant cells, dealing with the various molecular mechanisms and regulatory pathways involved and further dissecting the intricate balance of iron homeostasis and lipid peroxidation, highlighting the functioning of key proteins orchestrating this cell death pathway.
铁死亡是一种最近发现的细胞死亡机制，它与其他形式的程序性细胞死亡的区别在于脂质活性氧（ROS）的铁控制积累。铁死亡最初在动物中得到阐述，最终在植物细胞中也被发现，它与动物系统具有多个共同特征。植物中的这种细胞死亡途径与铁稳态机制相关，铁稳态机制对于调节铁的双重性质（既是必需的又是潜在有毒的）至关重要。与植物铁死亡相关的关键要素包括脂质代谢酶、铁螯合剂、ROS清除系统以及谷胱甘肽和抗坏血酸的耗尽。铁死亡导致的细胞死亡由脂质过氧化物的产生和线粒体收缩辅助。然而，应用铁死亡抑制剂，包括铁抑素-1和环吡酮胺，可以通过抑制脂质过氧化物和ROS的积累来阻碍细胞损伤。此外，为了调节植物铁死亡，信号通路以及对氧化应激和铁敏感的转录因子也很关键。植物中的铁死亡是一条复杂的途径，在细胞水平上由各种区室组成，如叶绿体、线粒体和细胞质。由于植物系统具有明确的代谢机制和显著的区室化程度，其独特性进一步增加了铁死亡轨迹的复杂性。因此，本综述深入探讨了目前对植物细胞中铁死亡的理解，涉及各种分子机制和调节途径，并进一步剖析铁稳态和脂质过氧化的复杂平衡，突出了协调这条细胞死亡途径的关键蛋白质的功能。
