STAT1 and diabetic neuropathy: Mechanistically, estrogen receptor alpha induced SIRT1 expression, which then deacetylates and activates AKT and STAT3, resulting in suppression of autophagy and adipogenesis via mTOR-ULK1 and p55 cascades.131 Moreover, HDAC4-STAT1 signaling-regulating autophagy inhibition is partially responsible for podocyte injury during diabetic neuropathy, in which STAT1 is deacetylated by HDAC4 to promote its phosphorylation and activation, which then translocates into the nucleus to induce gene expression, leading to the induction of inflammation and apoptosis and the suppression of autophagy.132