ReviewMolecular neurobiology2026
Therapeutic Timing at Mitochondrial Redox-Autophagy-Mitophagy Checkpoints in Age-Related Hearing Loss.
Review in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
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Abstract
Age-related hearing loss (ARHL) is common, disabling, and still managed largely with compensatory devices rather than mechanism-modifying therapy. The major weakness in the current translational pipeline is not the absence of candidate pathways, but the lack of a timing framework that links cochlear phenotype, mitochondrial injury state, and intervention intensity. This revised Review therefore focuses on a staged mitochondrial redox-quality-control model. We argue that ARHL emerges when high-energy cochlear compartments-outer and inner hair cells, spiral ganglion neurons, and the lateral wall/stria vascularis-cross a threshold at which mitochondrial reactive oxygen species (ROS), impaired mitochondrial DNA and transfer RNA integrity, lysosomal insufficiency, and incomplete mitophagy reinforce each other. Three checkpoints are emphasized because they are mechanistically actionable and experimentally measurable: NAD
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