Replicative senescence is the irreversible ceasing of cell division. It is an evolutionarily conserved cellular process that has been studied in different organisms. Different factors, including DNA damage and environmental stressors, such as oxidative stress, can induce senescence. Replicative senescence is a fundamental cellular phenomenon, which is linked to major disease-related processes, including cancer formation and progression, tissue repair, and organismal aging.
Replicative senescence is accompanied by numerous membrane- related phenotypic changes. Several studies have associated structural and compositional changes in fatty acids and sphingolipids with organismal aging.
In their brand new work, Lizardo DY and co-workers (2017) used an integrative lipidomics and transcriptomics approach for investigating the changes in lipids and lipid-related transcripts during replicative senescence in BJ fibroblasts.
Their results clearly show that specific triacylglycerols (TAGs) accumulate during replicative senescence. Previous studies have linked TAG accumulation to senescence in plants and yeast. To our knowledge, their analyses, for the first time, link involvement of TAGs to mammalian replicative senescence.
Their results demonstrate that TAG accumulation is very specific: TAG species with unsaturated, long and very long fatty acyl chains accumulate during replicative senescence. This structural specificity of the lipid species that change during replicative senescence suggests that PUFA–TAGs might have distinct roles in this process.
They also detected a big increase in the expression level of CD36, suggesting that increased fatty acid uptake mediated by CD36 could be responsible for the accumulation of PUFA–TAGs during replicative senescence.
Another fundamental aspect of mammalian cells influenced by lipids. Again.