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Issue 3, 2017
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Regulation of lipids is central to replicative senescence

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Cellular replicative senescence, a state of permanent cell-cycle arrest, has been linked to organismal aging, tissue repair and tumorigenesis. In this study, we comparatively investigated the global lipid profiles and mRNA content of proliferating and senescent-state BJ fibroblasts. We found that both expression levels of lipid-regulating genes and the abundance of specific lipid families, are actively regulated. We further found that 19 specific polyunsaturated triacylglycerol species constituted the most prominent changes in lipid composition during replicative senescence. Based on the transcriptome analysis, we propose that the activation of CD36-mediated fatty acid uptake and diversion to glycerolipid biosynthesis could be responsible for the accumulation of triacylglycerols during replicative senescence. This, in turn, could be a cellular mechanism to prevent lipotoxicity under increased oxidative stress conditions observed in this process. Our results indicate that regulation of specific lipid species has a central role during replicative senescence.

Graphical abstract: Regulation of lipids is central to replicative senescence

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The article was received on 13 Dec 2016, accepted on 17 Jan 2017 and first published on 19 Jan 2017

Article type: Paper
DOI: 10.1039/C6MB00842A
Citation: Mol. BioSyst., 2017,13, 498-509
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    Regulation of lipids is central to replicative senescence

    D. Y. Lizardo, Y. Lin, O. Gokcumen and G. E. Atilla-Gokcumen, Mol. BioSyst., 2017, 13, 498
    DOI: 10.1039/C6MB00842A

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