Abstract
Ferroptosis, a newly discovered form of regulatory cell death (RCD), has been demonstrated to be distinct from other types of RCD, such as apoptosis, necroptosis, and autophagy. Ferroptosis is characterized by iron-dependent lipid peroxidation and oxidative perturbation, and is inhibited by iron chelators and lipophilic antioxidants. This process is regulated by specific pathways and is implicated in diverse biological contexts, mainly including iron homeostasis, lipid metabolism, and glutathione metabolism. A large body of evidence suggests that ferroptosis is interrelated with various physiological and pathological processes, including tumor progression (neuro)degenerative diseases, and hepatic and renal failure. There is an urgent need for the discovery of novel effective ferroptosis-modulating compounds, even though some experimental reagents and approved clinical drugs have been well documented to have anti- or pro-ferroptotic properties. This review outlines recent advances in molecular mechanisms of the ferroptotic death process and discusses its multiple roles in diverse pathophysiological contexts. Furthermore, we summarize chemical compounds and natural products, that act as inducers or inhibitors of ferroptosis in the prevention and treatment of various diseases. Herein, it is particularly highlighted that natural products show promising prospects in ferroptosis-associated (adjuvant) therapy with unique advantages of having multiple components, multiple biotargets and slight side effects.
Highlights
Along with other biological processes, cell death is of great significance in various molecular physiological processes of mammalian development, homeostasis and disease (Thompson, 1995; Fuchs and Steller, 2011)
In 2007, Yagoda et al determined mitochondrial voltage-dependent anion channels 2 and 3 (VDAC2/3) as specific targets of erastin and VDAC2/3 induced a non-apoptotic cell death, which depends on the RASRAF-MEK pathway (Yagoda et al, 2007)
As numerous studies have reported, ferroptosis usually refers to a novel iron-dependent, lipid peroxidation-driven regulatory cell death (RCD), that is obviously distinct from apoptosis, necrosis and autophagy at the morphological, biochemical, and genetic levels (Xie et al, 2016a; Stockwell et al, 2017)
Summary
Along with other biological processes, cell death is of great significance in various molecular physiological processes of mammalian development, homeostasis and disease (Thompson, 1995; Fuchs and Steller, 2011).
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