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Where estrogen helps maintain the existing architecture of synaptic networks, GLP-1 signaling supports the biological machinery that allows those networks to adapt, strengthen, and repair
The entry of cisplatin into the inner ear leads to the formation of inner ear cellular damage products (DAMPs), which, together with cisplatin, bind to toll-like receptors (TLRs) (Babolmorad et al., 2021) and activate downstream signaling, producing transcription factors (e.g., nuclear factor kappa B (NF-B), activator protein-1 (AP-1), and interferon regulatory factor 3 (IRF3)), which in turn regulate the expression and secretion of proinflammatory signaling molecules
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Elevation of intracellular Ca 2+ activates scramblase to ensure PS externalization, opens the Gardos channels, resulting in K + efflux and subsequent cell shrinkage, and mobilizes calpain, leading to cytoskeleton degradation and membrane microvesiculation [78]
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