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In erythrocytes, GSH has been implicated in reactions which maintain the native structure of hemoglobin and of enzymes and membrane proteins
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MAFbx/Atrogin-1 and MuRF-1 are shown to be increased in various muscle atrophy-inducing conditions, including disuse, denervation, inflammation, aging, glucocorticoid increase, high Ang II, and chronic diseases such as cancer, congestive heart failure, chronic kidney disease, chronic obstructive pulmonary disease (COPD), and AIDS [31,32]
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