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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.
Ferroptosis, a cell death mechanism induced by lipid peroxidation, is pivotal in tumor suppression. A recent study shows that tumor repopulating cells evade ferroptosis and develop resistance to therapy via subverting a lipid metabolism enzyme.
Phosphorylation of ACSL4 by mitochondria-located metabolic kinase PCK2 is critical to regulating ferroptosis-associated phospholipid remodeling in tumor-repopulating cells that are resistant to chemotherapy and radiotherapy.
Sleep disorders increase the risk and mortality of heart disease. Here, the authors show that sleep fragmentation results in elevated copper levels in the male mouse heart and exacerbates myocardial ischemia–reperfusion injury with increased myocardial cuproptosis and apoptosis.
Here the authors structurally and mechanistically characterize the assembly of FADD, procaspase-8, and cFLIP through their death-effector domains (DEDs), providing insights into the regulation of apoptotic and necroptotic signalling.
Ferroptosis, a cell death mechanism induced by lipid peroxidation, is pivotal in tumor suppression. A recent study shows that tumor repopulating cells evade ferroptosis and develop resistance to therapy via subverting a lipid metabolism enzyme.
Reversible S-palmitoylation regulates gasdermin D cleavage, membrane translocation and pore formation to control pyroptosis following bacterial infection.
Diverse, specialized immune cells defend against pathogens and cancer cells. A new study reveals the comprehensive lipid compositions of these cells, with unique lipidomes associated with various immune cell types. They show that cell-specific lipid compositions determine a key functional phenotype: their susceptibility to ferroptosis.
Detection of intracellular lipolysaccharide (LPS) activates an immune response initiated by the non-canonical inflammasome. ATGL has now been identified as a negative regulator of this pathway that dampens inflammation by removing LPS’ acyl chains, preventing the activation of inflammatory caspases and cytokines.