Hormonal
Inhibition of sphingolipid synthesis (specifically via SPT inhibition by myriocin or CerS inhibition by fumonisin B1) extends lifespan in model organisms like yeast and C. elegans, suggesting that reducing ceramide production can delay aging.
Research in simple organisms shows that reducing the production of certain lipids (sphingolipids) can extend lifespan. This suggests that metabolic pathways involving lipid synthesis are key regulators of aging. For humans, this points to the importance of metabolic health and lipid balance, though direct application of inhibitors like myriocin is not currently a standard human intervention.
Deletion of a gene coding for CerS (longevity-assurance gene 1, LAG1) results in an increase of mean and maximum lifespan... Downregulation of sphingolipid synthesis induces an increase of lifespan, shown by lowering the expression of the SPT subunits LCB1 and LCB2, or by using the SPT pharmacological inhibitor Myr.
Why this rating
Consistent findings across multiple model organisms (yeast, worms, flies) support the link between sphingolipid reduction and lifespan extension.
Source
Role of sphingolipids in senescence: implication in aging and age-related diseases
Magali Trayssac et al. · Journal of Clinical Investigation · 2018
DOI 10.1172/jci97949
More from this paper
- Elevated intracellular ceramide levels induce cellular senescence and contribute to age-related pathologies such as insulin resistance and atherosclerosis, whereas sphingosine-1-phosphate (S1P) delays senescence and promotes cell survival.Good
- Ceramide accumulation in specific tissues (adipose, liver, muscle) during aging and high-fat diet consumption drives insulin resistance and inflammation, linking sphingolipid metabolism to type 2 diabetes.Good
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