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Interestingly, ABHD5 mutations causative in CDS do not co-localize to LDs and are unable to stimulate PNPLA2 lipolytic activity (30), demonstrating an important function for the interaction in the etiology of CDS and lipid storage

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Results showed that the ingredient significantly increased NAD+ levels in senescent fibroblasts, activated the SIRT1 signaling pathway, reduced the expression of senescence-associated -galactosidase (SA--gal), decreased intracellular reactive oxygen species accumulation, and promoted collagen synthesis

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