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Here, we identify dysregulated mitochondrial dynamics as a key driver of HS and develop a new targeted therapy. Specifically, excessive mitochondrial fission was observed in macrophages derived from both human and murine HS tissues. In vitro and in vivo experiments revealed that this imbalance is governed by AURKB\u2010mediated phosphorylation of DRP1 at Ser616 site. Through machine\u2010learning coupled with biological validation, we identified the natural small\u2010molecule Asiaticoside (AS) as a potent AURKB inhibitor. However, AS has limited targeting accuracy and poor bioavailability. To overcome these challenges, we developed cRGD\u2010decorated extracellular vesicles\u00a0(EVs) loaded with AS (AS@cRGD\u2010EVs), enabling targeted delivery of AS to macrophages within wound tissue. In vitro and in vivo studies showed that AS@cRGD\u2010EVs effectively restrained macrophage mitochondrial fission, rebalanced the inflammatory milieu, and conferred significant anti\u2010scarring efficacy in murine HS models. This work establishes mitochondrial dynamics as a therapeutic axis for HS and delivers a targeted nanotherapeutic ready for translational evaluation.<\/jats:p>","DOI":"10.1002\/advs.202517108","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T19:02:42Z","timestamp":1770231762000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Targeted Extracellular Vesicles Deliver Asiaticoside to Inhibit AURKB\/DRP1\u2010Mediated Mitochondrial Fission and Attenuate Hypertrophic Scar Formation"],"prefix":"10.1002","volume":"13","author":[{"given":"Luyu","family":"Li","sequence":"first","affiliation":[{"name":"Department of Dermatology Shanghai Ninth People's Hospital Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenli","family":"Si","sequence":"additional","affiliation":[{"name":"Department of Dermatology 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