All articles tagged with #lipidomics
A study in Nature Aging identifies the lengthening of lipid acyl chains as a conserved hallmark of aging in mice, worms, flies, and humans. The research links this molecular shift to the gene Plb1, which regulates lipid remodeling. Interventions that shorten lipids, such as dietary restriction or genetic knockdown, extend lifespan, suggesting a causal link between lipid chain length and longevity.
A Nature Metabolism study shows lipids in ovarian cancer ascites rewire T cell membranes and metabolism, notably 18:0–18:2 phosphatidylcholine, which impairs T cell activation by disrupting nanoscale TCR clustering in the immunological synapse. These lipids alter membrane order and TCR recycling, reducing activation at physiological concentrations; pre-activated T cells can overcome the barrier, pointing to strategies to improve adoptive T cell therapies for ovarian cancer.
New research from the Leibniz Institute on Aging links age-related mitochondrial decline to reduced membrane phosphatidylcholine, which makes mitochondrial networks more fragmented and less adaptable. In Caenorhabditis elegans, impairing phosphatidylcholine production induced aging-like mitochondrial changes, while providing phosphatidylcholine or its precursor choline restored youthful mitochondrial structure and function within two days. The study integrated worm experiments, human cell data, and aging datasets, suggesting that lipid changes—not just genetic damage—drive mitochondrial aging and that dietary or metabolic interventions could modestly slow aging, though translation to humans requires further work.
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.
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.