All articles tagged with #ferroptosis
Researchers find that riboflavin (vitamin B2) metabolism supports cancer cells' defenses against ferroptosis, an iron-driven form of cell death, via the FSP1 pathway. Lowering B2 metabolism could make tumors more susceptible to ferroptosis, and roseoflavin—an Anthrobacter-derived compound—triggers ferroptosis in cancer cells at low doses, suggesting a potential therapeutic approach, though specific inhibitors are not yet available.
Dietary lipid composition (PUFAs/MUFAs) determines mouse T cell resistance to ferroptosis, shaping T cell homeostasis and immune responses via lipid remodeling; these diet‑induced ferroptosis effects (DEFs) are microbiota‑independent and correlate with human plasma lipid profiles, with PUFA‑containing phospholipids driven by ACSL4 underpinning TFH cell development and broader T cell–mediated immunity, including anti‑tumor responses and CAR‑T therapy. The findings suggest targeting lipid metabolism could enhance vaccines and immunotherapies.
Researchers have uncovered how a rare genetic mutation in the GPX4 gene causes neurodegeneration through ferroptosis, a form of cell death linked to oxidative damage, providing new insights into diseases like Alzheimer's and childhood dementia.
The study reveals that the lymph node microenvironment promotes resistance to ferroptosis in metastasizing melanoma by downregulating GSH synthesis and upregulating FSP1, which localizes to lysosomes and provides a GPX4-independent protective mechanism. Oxygen levels and epigenetic regulation influence GPX4 stability and ferroptosis sensitivity, suggesting potential therapeutic strategies targeting FSP1 and GSH synthesis in LN metastases.
Targeting FSP1 induces ferroptosis, a form of cell death, in lung cancer models, suggesting FSP1 as a promising therapeutic target for treating lung cancer by promoting tumor cell ferroptosis.
The study reveals that female kidney tissues are resistant to ferroptosis and acute kidney injury due to the protective effects of oestradiol, which acts through non-genomic antioxidant mechanisms and ESR1-dependent pathways, while male tissues are more susceptible due to higher ether lipid plasticity and lower hydropersulfide levels.
US researchers discovered that cancer cells use sugar-coated molecules called GAGs to steal fat-rich lipoproteins carrying vitamin E from the bloodstream, which helps them avoid ferroptosis, a form of cell death. Blocking this pathway could open new avenues for cancer treatment, although clinical applications are still in the future.
D-FW researchers discovered that cancer cells use lipoproteins and sulfated glycosaminoglycans to shield themselves from ferroptosis by importing vitamin E, an antioxidant, which helps them survive. Disrupting this pathway could lead to new cancer treatments, although clinical applications are still in the future.
Researchers at Columbia University have identified a rare lipid, diPUFA phospholipid, as a crucial factor in promoting ferroptosis, a unique form of cell death. This discovery has significant implications for treating neurodegenerative diseases and cancer, as it opens new avenues for either preventing or inducing cell death. The interdisciplinary research involved the Department of Biological Sciences, Department of Chemistry, and the Columbia University Irving Medical Center, and the findings deepen our understanding of ferroptosis and its potential for controlling cell death.
A study has found that 7-dehydrocholesterol, a precursor to cholesterol, plays a crucial role in determining the sensitivity of cells to ferroptosis, a form of cell death. The research, which utilized CRISPR screening and lipidomic analysis, provides insights into the mechanisms underlying ferroptosis and its potential implications for various diseases. The data from the study are available online, contributing to the accessibility and reproducibility of the findings.
Researchers have discovered that 7-dehydrocholesterol (7-DHC), a molecule used to make cholesterol, acts as a defense against ferroptosis, a form of regulated cell death. This finding could lead to new treatments for cancer and other clinical conditions, shedding light on the underpinnings of cell protection mechanisms.
A study has identified 7-dehydrocholesterol as a natural inhibitor of ferroptosis, a form of cell death driven by lipid peroxidation. The research sheds light on the role of 7-dehydrocholesterol-derived oxysterols in regulating ferroptosis sensitivity and provides insights into the mechanisms of this type of cell death. The data and materials supporting the findings are available in the main text, figures, and extended data figures, as well as in a repository for (epi)lipidomics experiments.
Scientists have discovered a small molecule called N6F11 that induces ferroptosis, a unique form of cell death, to selectively kill various cancers while sparing immune cells. Ferroptosis relies on iron buildup and the generation of reactive oxygen species to trigger cell death. Current cancer treatments often rely on apoptosis, but many tumors have developed resistance to this form of cell death. N6F11 shows promise in degrading a protein called GPX4, which blocks ferroptosis, and has been found to slow tumor growth in mouse models without severe side effects. Further research is needed to evaluate the potential of N6F11 as a cancer treatment.
Researchers from the Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) in Bengaluru have discovered that plant-based polyphenols, such as tannic acid found in trees like Chestnut and Oak, could be a cost-effective strategy for combating Alzheimer's disease (AD). The study found that these polyphenols have the potential to ameliorate ferroptosis, a form of programmed cell death associated with AD, by activating and enhancing the GPX4 pathway. The findings offer new avenues for targeting novel pathways in the development of therapeutics for AD and may inspire the exploration of natural compounds for enhanced efficacy against neurodegenerative diseases.
Researchers have discovered a new form of cell death called ferroptosis, triggered by iron accumulation, which destroys microglia cells in Alzheimer's disease and vascular dementia. The study found that microglia degenerates in the white matter of the brain while attempting to clear iron-rich myelin. This new insight into the role of microglial degeneration in neurodegenerative diseases could lead to the development of novel therapeutic interventions.