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Shifting CrAT activity towards the production of acetylcarnitine may rescue beta-oxidation by increasing free CoA, but it only partially solves problems of energy deficiency because the acetyl groups do not enter the Krebs cycle for energy production, but rather escape from the mitochondria in the form of acetylcarnitine

AMPK inhibits mTORC1 shortly after mitochondrial dysfunction begins, whereas HRI do so at later stages

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