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Specific activation of mTORC1 in the podocytes in DKD leads to many changes in DKD, including increased albuminuria, podocyte loss, and thylakoid membrane expansion, while AMPK in DKD decreased autophagic activity in podocytes and increased cytotoxicity and apoptosis (157, 158)
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However, pathological levels of ROS disable the mechanisms responsible for maintaining the reversibility of S-nitrosylation inducing a cellular state described as protein hypernitrosylation [202]
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