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The echolocating bats exhibit natural resistance to intense noise, and this suggested novel insights into methods to protect against NIHL. Here, through comparative transcriptomic analysis of noise\u2010exposed cochleae from the eastern bent\u2010winged bats (\n                    <jats:italic>Miniopterus fuliginosus<\/jats:italic>\n                    ) and mice, the specific transcriptional dynamics in noise\u2010resistant\n                    <jats:italic>Miniopterus fuliginosus<\/jats:italic>\n                    are revealed, thus highlighting potential mechanisms for preventing cochlear damage that mouse models cannot replicate, with\n                    <jats:italic>Hras<\/jats:italic>\n                    emerging as the most significant hub upregulator. Functional validation in mice demonstrates that HC\u2010specific Hras overexpression significantly attenuates noise\u2010induced HC death, synaptic loss, and auditory threshold shifts. Mechanistically, Hras confers protection by activating the PI3K\/Akt signaling pathway, a critical pro\u2010survival cascade. The findings further disentangle the mechanisms of cochlear resistance to intense noise in echolocating bats and suggest that targeting Hras expression may be a potential therapeutic intervention against NIHL.\n                  <\/jats:p>","DOI":"10.1002\/advs.202508466","type":"journal-article","created":{"date-parts":[[2025,9,8]],"date-time":"2025-09-08T11:38:56Z","timestamp":1757331536000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Comparative Cochlear Transcriptomics in Echolocating Bats and Mouse Reveals Hras as Protector Against Noise\u2010Induced Hearing Loss"],"prefix":"10.1002","volume":"12","author":[{"given":"Peng","family":"Chen","sequence":"first","affiliation":[{"name":"ENT Institute and Otorhinolaryngology Department of Eye &amp; ENT Hospital State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science Fudan University  Shanghai 200031 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