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Increasing levels of acetyl-CoA through either pathway has the potential to strongly deplete the levels of CoA needed in the mitochondrial matrix for beta oxidation of fatty acids

Preclinical studies have demonstrated that TMAO can induce apoptosis in various target cells, such as human aortic vascular smooth muscle cells, 158 pancreatic acinous cells, renal tubular epithelial cells, 159 human aortic endothelial cells, 160,161 and neurons, 119 contributing to the development and progression of cardiovascular, renal, neurological, and pancreatic diseases

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Mayo, K