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A permissive apoptotic environment: function of a decrease in intracellular superoxide anion and cytosolic acidification
In PNA mice, GLP1/E therapy caused upregulation of pathways involved in the metabolism of non-coding RNA, estrogen-dependent gene expression, autophagy, vesicle-mediated transport, and signaling by nuclear receptors, whereas proteins related to inflammation (ROS and RNS production in phagocytes), cellular response to starvation, signaling by insulin receptor, apoptosis, and immune system were downregulated
It is triggered by the GTPases mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2), located in the OMM
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