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NMNAT1 Activates Autophagy to Delay D-Galactose-Induced Aging in Cochlear Hair Cells
Yongjie Wei1, Wenqing Yang1, Han Wu1
1Department of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Aging Cell
|January 12, 2026
Summary
Nicotinamide nucleotide adenylate transferase 1 (NMNAT1) slows cochlear hair cell aging by activating autophagy and regulating metabolism. This discovery presents NMNAT1 as a promising therapeutic target for age-related hearing loss (ARHL).
Area of Science:
- Otolaryngology
- Cellular Biology
- Metabolomics
Background:
- Age-related hearing loss (ARHL) incidence is rising with an aging population.
- Cellular aging is linked to reduced nicotinamide adenine dinucleotide (NAD+) and impaired autophagy, but mechanisms are unclear.
- Cochlear hair cell aging is a key factor in ARHL.
Purpose of the Study:
- To investigate the role of nicotinamide nucleotide adenylate transferase 1 (NMNAT1) in cochlear hair cell aging.
- To explore NMNAT1's impact on autophagy and metabolic pathways in aging hair cells.
Main Methods:
- Utilized D-galactose (D-gal)-induced aging HEI-OC1 cells and cochlear explants.
- Assessed NMNAT1 expression and its modulation effects.
- Performed metabolomic analysis on Nmnat1-knockout cells.
Main Results:
- D-gal treatment significantly reduced NMNAT1 expression in hair cells.
- NMNAT1 overexpression enhanced autophagy and slowed hair cell aging.
- Metabolomic analysis revealed tricarboxylic acid cycle dysregulation in Nmnat1-knockout cells.
Conclusions:
- NMNAT1 plays a crucial role in regulating autophagy and metabolic pathways during hair cell aging.
- NMNAT1 influences age-related changes in cochlear hair cells.
- NMNAT1 is identified as a potential therapeutic target for preventing and treating ARHL.
