Urolithin A prevents age-related hearing loss in C57BL/6J mice likely by inducing mitophagy.

Sung Il Cho, Eu-Ri Jo, Hee Sun Jang

Department of Otolaryngology-Head and Neck Surgery, Chosun University College of Medicine, Gwangju, Republic of Korea. Electronic address: [email protected] of Otolaryngology-Head and Neck Surgery, Chosun University College of Medicine, Gwangju, Republic of Korea. Electronic address: [email protected]. · pubmed

Paper

Abstract

Mitochondrial dysfunction with aging is associated with the development of age-related hearing loss. Mitophagy is a cardinal mechanism to maintain a healthy mitochondrial population through the turnover of damaged mitochondria. Declining mitophagy with age causes a buildup of damaged mitochondria, leading to sensory organ dysfunction. The effect of Urolithin A (UA), a mitophagy inducer, was investigated on age-related hearing loss in a mouse model. C57BL/6J mice were treated with UA from 6 to 10 months of age. UA attenuated an auditory brainstem responses (ABR) threshold shift at 8, 16, and 32 kHz frequencies, and improved mitochondrial DNA integrity and ATP production in the cochlea and auditory cortex. The mRNA levels of mitophagy-related genes and protein levels of PINK1, Parkin, BNIP3, and LC3B increased in the cochlea and auditory cortex. The expression of mitophagosomes and mitophagolysosomes in the cochlea, spiral ganglion, auditory cortex, and inferior colliculus increased, together with the expression of Parkin and BNIP3 in the cochlea, spiral ganglion, auditory cortex, and inferior colliculus. These results indicate that UA counteracted mitophagy decline in the auditory system and prevented age-related hearing loss. UA can be used as a potential agent to prevent age-related hearing loss.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper addresses the decline of mitophagy with aging, which is a fundamental aspect of cellular aging and mitochondrial dysfunction. By investigating Urolithin A as a potential agent to induce mitophagy and prevent age-related hearing loss, the study contributes to understanding mechanisms that could mitigate age-related decline. However, while the findings are solid, they primarily focus on a specific application rather than providing broad insights that could significantly advance the field of longevity research. Thus, the impact is rated as limited but still meaningful.

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