Vitamin E/Coenzyme Q-Dependent "Free Radical Reductases": Redox Regulators in Ferroptosis.
Antioxid Redox Signal
; 40(4-6): 317-328, 2024 02.
Article
in En
| MEDLINE
| ID: mdl-37154783
ABSTRACT
Significance:
Lipid peroxidation and its products, oxygenated polyunsaturated lipids, act as essential signals coordinating metabolism and physiology and can be deleterious to membranes when they accumulate in excessive amounts. Recent Advances There is an emerging understanding that regulation of polyunsaturated fatty acid (PUFA) phospholipid peroxidation, particularly of PUFA-phosphatidylethanolamine, is important in a newly discovered type of regulated cell death, ferroptosis. Among the most recently described regulatory mechanisms is the ferroptosis suppressor protein, which controls the peroxidation process due to its ability to reduce coenzyme Q (CoQ). Critical Issues In this study, we reviewed the most recent data in the context of the concept of free radical reductases formulated in the 1980-1990s and focused on enzymatic mechanisms of CoQ reduction in different membranes (e.g., mitochondrial, endoplasmic reticulum, and plasma membrane electron transporters) as well as TCA cycle components and cytosolic reductases capable of recycling the high antioxidant efficiency of the CoQ/vitamin E system. Future Directions We highlight the importance of individual components of the free radical reductase network in regulating the ferroptotic program and defining the sensitivity/tolerance of cells to ferroptotic death. Complete deciphering of the interactive complexity of this system may be important for designing effective antiferroptotic modalities. Antioxid. Redox Signal. 40, 317-328.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Ubiquinone
/
Ferroptosis
Language:
En
Journal:
Antioxid Redox Signal
Journal subject:
METABOLISMO
Year:
2024
Type:
Article
Affiliation country:
United States