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This perspective is reinforced by the central gain model of tinnitus, which suggests that tinnitus results from an abnormal compensatory increase in gain (i.e., neural amplification) within the CAS to compensate for a loss of sensory input from the cochlea 9,10,11
Extracellular relay and paracrine propagation Although direct membrane contacts and ROS-triggered waves provide two compelling frameworks for ferroptotic spread, neither fully explains how ferroptosis extends across anatomically separated yet functionally coupled cells
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Alongside their peroxidase activity, they may also function as molecular chaperones [45] and specific oxidases in signaling pathways through redox relay reactions [46,47]
