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Additionally, when activated, the SAPK/JNK pathway can trigger the P53-YAP1 pathway, decrease GPX4 levels, promote ROS accumulation, and increase susceptibility to ferroptosis [134-136]

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GIPR antagonism and GLP-1R agonism both modulate DVC gene programmes implicated in synaptic plasticity We next performed cell-type prioritization analysis using Augur 42 to determine which types of neurons were most affected by individual drug treatment in the DVC (Fig