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Cell death terminates normal cellular functions, including respiration, metabolism, growth and proliferation. Cell death can be non-programmed, for example as the result of accidental injury or trauma, or programmed. Types of programmed cell death include anoikis, apoptosis, autophagy, necrosis, necroptosis and pyroptosis.
Two independent studies published in Nature implicate distal cholesterol biosynthesis in the regulation of ferroptosis and show that 7-dehydrocholesterol (7-DHC) is an endogenous, anti-ferroptotic metabolite.
Selenium is usually incorporated into selenoproteins, with important functions in redox regulation. A new study in Nature Metabolism reveals a previously unappreciated role for selenium-based chemical species as direct electron donors to reduce ubiquinone, thus contributing to redox homeostasis by preventing lipid peroxidation.
Half a century after its discovery, platelet-activating factor (PAF) is now recognized as a ferroptosis-activating phospholipid that contributes to tubule cell damage and nephron loss in acute kidney injury.