CNS neuroscience & therapeutics · 2026
Application of a Combined Transcriptomics and Proteomics Analysis Approach to Explore Potential Mechanisms of Biomarkers in NIHL.
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Ding Zhong-Jia, Tian Chao-Yong, Wang Ren-Feng, Wang Yin, Zha Ding-Jun
Аннотация
OBJECTIVE: This study aimed to elucidate the molecular mechanisms underlying noise-induced hearing loss (NIHL) by analyzing cochlear protein expression and transcriptional profiles at multiple time points after noise exposure. This investigation aimed to identify key biomarkers and potential therapeutic targets to mitigate the irreversible effects of NIHL.
METHODS: Cochlear specimens were collected from animal models at 1, 14, and 28 days post-noise exposure. Integrated transcriptomic and proteomic analyses were performed to identify differentially expressed genes and proteins, followed by bioinformatic analyses to explore their functional roles. Reverse transcription quantitative PCR (RT-qPCR) was used to validate the expression levels of selected genes.
RESULTS: Six biomarkers (Gm37065, Cd5l, F930017D23Rik, Eldr, Gm30948, and Tspo2) showed strong correlations with NIHL. RT-qPCR validation revealed a significant decrease in mRNA expression of five of these genes, including Gm37065, across all experimental groups, while the expression of Cd5l remained unchanged. Functional analyses indicated that disruptions in mitochondrial energy metabolism and cochlear inflammation are key contributors to NIHL pathogenesis.
CONCLUSION: This study reveals dynamic molecular changes associated with NIHL progression and identifies novel biomarkers and pathways with potential therapeutic relevance. Further mechanistic validation and functional studies are necessary to elucidate the roles of Tspo, Cd5l, and other identified molecules in NIHL pathogenesis and to develop targeted therapeutic strategies.
METHODS: Cochlear specimens were collected from animal models at 1, 14, and 28 days post-noise exposure. Integrated transcriptomic and proteomic analyses were performed to identify differentially expressed genes and proteins, followed by bioinformatic analyses to explore their functional roles. Reverse transcription quantitative PCR (RT-qPCR) was used to validate the expression levels of selected genes.
RESULTS: Six biomarkers (Gm37065, Cd5l, F930017D23Rik, Eldr, Gm30948, and Tspo2) showed strong correlations with NIHL. RT-qPCR validation revealed a significant decrease in mRNA expression of five of these genes, including Gm37065, across all experimental groups, while the expression of Cd5l remained unchanged. Functional analyses indicated that disruptions in mitochondrial energy metabolism and cochlear inflammation are key contributors to NIHL pathogenesis.
CONCLUSION: This study reveals dynamic molecular changes associated with NIHL progression and identifies novel biomarkers and pathways with potential therapeutic relevance. Further mechanistic validation and functional studies are necessary to elucidate the roles of Tspo, Cd5l, and other identified molecules in NIHL pathogenesis and to develop targeted therapeutic strategies.