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doi: 10.1111/bdi.12652

The increased accumulation of acetyl-CoA in mitochondria of diabetic hearts, due to increases in FA metabolism, may account for increased acetylation levels.38 Conversely, NAD + is a co-factor for SIRT3 deacetylation, and so decreased free NAD + concentrations, as have been reported in the T2D heart, could decrease SIRT3 activity and level of deacetylation

Those released in a healthy context may support neuronal homeostasis, whereas vesicles from stressed or diseased cells often propagate pathology [17,33]