Abstract
The induction and consequences of regulated cell death (RCD) are accompanied by changes in gene and protein expression, biochemical pathways, as well as cell morphology and size. Such RCDs have a significant impact on development, tissue homeostasis, and the occurrence and progression of disease. Among different forms of RCD, ferroptosis appears to be the main cause of tissue damage driven by iron overload and lipid peroxidation. In fact, the dysfunctional ferroptotic response is implicated in a variety of pathological conditions and diseases, such as neurodegenerative diseases, tissue ischemia-reperfusion injury, tumorigenesis, infections, and immune diseases. Ferroptotic response can be fine-tuned through various oxidative stress and antioxidant defense pathways, coupling with metabolism, gene transcription, and protein degradation machinery. Accordingly, a series of ferroptosis inducers or inhibitors targeting redox- or iron metabolism-related proteins or signal transduction have been developed. Although this kind of RCD has recently attracted great interest in basic and clinical research, detecting and monitoring a ferroptotic response still faces challenges. In this mini-review, we not only summarize the latest knowledge about the characteristics of ferroptosis in vitro and in vivo, but also discuss the specificity and limitations of current biomarkers of ferroptosis.
Highlights
Cell death is a basic biological process that regulates cell fate, tissue regeneration, and the body’s immune response
The production of polyunsaturated fatty acids (PUFAs) for subsequent lipid peroxidation requires the activation of several upstream lipid synthesis and metabolism pathways, especially acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated conversion of arachidonic acid (AA) to AA-CoA (Yuan et al, 2016b; Doll et al, 2017; Kagan et al, 2017)
GPX4independent anti-ferroptosis pathway relies on the production of coenzyme Q10 (CoQ10) (Bersuker et al, 2019; Doll et al, 2019) or BH4 (Kraft et al, 2020; Soula et al, 2020), which is further regulated by apoptosis inducing factor mitochondria associated 2 (AIFM2/FSP1) or GTP cyclohydrolase 1 (GCH1), respectively
Summary
Reviewed by: Jingfang Ju, Stony Brook Medicine, United States Xiao-Ming Yin, Tulane University, United States. The induction and consequences of regulated cell death (RCD) are accompanied by changes in gene and protein expression, biochemical pathways, as well as cell morphology and size Such RCDs have a significant impact on development, tissue homeostasis, and the occurrence and progression of disease. A series of ferroptosis inducers or inhibitors targeting redox- or iron metabolism-related proteins or signal transduction have been developed This kind of RCD has recently attracted great interest in basic and clinical research, detecting and monitoring a ferroptotic response still faces challenges. In this mini-review, we summarize the latest knowledge about the characteristics of ferroptosis in vitro and in vivo, and discuss the specificity and limitations of current biomarkers of ferroptosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
