Nature Aging：刘光慧/柴人杰等揭示二甲双胍有望助力老年性耳聋的防治

Core Viewpoint - The article discusses the significant public health challenge posed by age-related hearing loss, emphasizing the need for deeper understanding of the molecular mechanisms involved in cochlear aging, particularly in primates, to develop targeted treatment strategies [1][2]. Group 1: Research Findings - A collaborative research team published a study in Nature Aging, identifying SLC35F1 deficiency as a key molecular marker and driver of cochlear aging in primates [2][7]. - The study successfully mapped the cellular and molecular characteristics of cochlear aging, revealing critical pathological changes such as hair cell loss and accelerated aging of spiral neurons [4][7]. - The research utilized innovative techniques to dissect primate cochlear tissue and employed single-cell sequencing combined with deep learning to create a high-resolution molecular map of cochlear aging [4][6]. Group 2: Mechanism and Treatment - The study demonstrated that silencing SLC35F1 in hair cells leads to significant cell apoptosis, indicating its crucial role in maintaining hair cell homeostasis [6]. - Long-term administration of metformin showed a rejuvenating effect on aged cochlear tissue in primates, reducing hair cell loss and vascular degeneration, while also decreasing the proportion of aging neurons [6][7]. - Metformin was found to exert protective effects through dual mechanisms: downregulating inflammation-related genes and upregulating key functional genes related to sound perception and neural signaling [6][7]. Group 3: Implications for Future Research - The findings provide a comprehensive understanding of the aging process in primate cochlea, highlighting specific susceptible cell types and their aging drivers, which could lead to innovative targeted therapies for age-related hearing loss [7][8]. - The research lays a solid theoretical foundation for developing clinical intervention strategies aimed at preventing and treating age-related hearing loss [7].