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The gradual loss of longevity in MSCs triggers various cellular dysfunctions associated with aging including the accumulation of damaged DNA, epigenetic alterations, reactive oxygen species (ROS), mitochondrial dysfunctions as well as a profound loss of proteostasis, that collectively lead to cellular senescence and proliferation arrest [39]

In addition to insulin resistance and type-2 diabetes, C16:1 is implicated in mitochondrial permeability (Kurotani et al., 2012

Efficacy and safety of coenzyme Q10 supplementation in the treatment of polycystic ovary syndrome: a systematic review and meta-analysis

5 TMAO-mediated immunometabolism in IBD Emerging evidence highlights TMAOs dual role as both a biomarker of microbial-host metabolic crosstalk and a direct instigator of immune-inflammatory cascades, bridging gut dysbiosis to intestinal mucosal damage (86)