What organelles are involved in ferroptosis?

These are the main organelles involved in ferroptosis:

• Mitochondria play a major role in initiating and propagating ferroptosis by generating reactive oxygen species (ROS) as a byproduct of oxidative phosphorylation. During ferroptosis, these organelles undergo significant changes including reduced size, increased membrane density, reduced or absent cristae, and ruptured mitochondrial membrane. 
• Lysosomes are acidic membrane-bound organelles. They play a three-fold role in ferroptosis by activating autophagy, releasing lysosomal cathepsins, and accumulation of nitric oxide or lysosomal iron. 
• Endoplasmic Reticulum (ER) is the key organelle involved in lipid secretion and protein synthesis and processing. ER stress can initiate an unfolded protein response in an attempt to reestablish protein homeostasis but can also initiate cell death on failure to restore homeostasis. ER stress is also involved in ferroptosis via pathways like EIF2A/ATF4, which can increase resistance or susceptibility to ferroptosis. 
• Lipid Droplets (LDs) serve as storage organelles for neutral lipids. They also interact with other organelles to exchange lipids, ions, and metabolites. LD formation protects cells against ER stress and PUFA-induced lipotoxicity and ER stress. During the early stages of ferroptosis, the number of lipid droplets increases but in the final stages, the number drops. Sensitivity to ferroptosis is affected by the balance between the storage and degradation of lipid droplets. 
• Peroxisomes generate ROS and reactive nitrogen species (RNS). They also contain antioxidant enzymes. A recent study suggested that ferroptosis may be promoted by peroxisome-mediated lipid synthesis rather than generation of ROS or RNS.
• Golgi Apparatus is involved in processing and sorting lipids and proteins for cellular use. Certain pharmacological Golgi stress inducers can initiate ferroptosis in HeLa cells. Although the mechanism is not yet fully understood, it is thought that Golgi stress-induced ferroptosis might be due to loss of antioxidant molecules and impaired protein homeostasis.
• Although the nucleus is less directly involved, it participates in the overall regulation and signaling pathways influencing ferroptosis.