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TMAO contributes to disease progression through multiple mechanisms: on one hand, it promotes inflammation, enhances oxidative stress, exacerbates myocardial necrosis, and drives metabolic remodeling, ultimately inducing myocardial injury

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In cerebral organoids derived from these iPSCs, axonal mitochondria showed decreased stability and a shift toward retrograde orientation, resulting in a net reduction of mitochondrial density within the axon (88)

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