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This is consistent with the increased -KG content in myofibroblasts, as -KG activates mTORC1, which promotes the expression of collagen (224)

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In AP, mitochondrial dysfunction, including ATP depletion, mtROS overproduction, and loss of m, promotes nuclear activation of stress-responsive transcriptional programs that enhance cytokine and chemokine expression and thereby contribute to pancreatic inflammation ( ATF4 is a key effector of the integrated stress response that connects mitochondrial stress, ER stress, and redox imbalance to nuclear transcriptional reprogramming

This allows you to track how your body responds without overwhelming your system