Unraveling the complexity of ferroptosis in plants: Triggers, pathways, antioxidant system and connecting links.

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.