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Here, we developed a brain endothelial cell membrane\u2010coated ROS\u2010responsive biomimetic nanoplatform (NP@D+M) for co\u2010delivery of the VDAC1 inhibitor DIDS and the mitochondrial fission inhibitor Mdivi\u20101. NP@D+M showed uniform size, preserved endothelial membrane proteins, and accelerated drug release under elevated H2O2. In ICH\u2010like neuronal injury models, NP@D+M enhanced uptake, protected neurites, reduced LDH release and apoptosis, restored mitochondrial membrane potential and ATP production, and suppressed mitochondrial ROS. Mechanistically, NP@D+M disrupted aberrant LPAR1\u2010VDAC1 interaction, inhibited mPTP opening, and restored mitochondrial homeostasis; LPAR1 gain\u2010 and loss\u2010of\u2010function experiments confirmed its role in the mitochondrial protective effect. Targeted metabolomics and single\u2010cell transcriptomics further supported improved energy metabolism and attenuated injury\u2010associated cellular responses. In vivo, NP@D+M crossed the BBB, accumulated in brain parenchyma, protected perihematomal neurons, improved mitochondrial function, and alleviated neurological and cognitive deficits without obvious systemic toxicity. These findings identify a LPAR1\u2010VDAC1\u2010mPTP\u2010targeted nanotherapeutic strategy for mitochondrial protection and neural repair after ICH.<\/jats:p>","DOI":"10.1002\/advs.78075","type":"journal-article","created":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T03:23:37Z","timestamp":1791775417000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial Protection and Neural Repair via ROS\u2010Responsive Biomimetic Nanoparticles in Intracerebral Hemorrhage"],"prefix":"10.1002","author":[{"given":"Ling","family":"Gao","sequence":"first","affiliation":[{"name":"Haikou Research Institute of Xiangya School of Medicine Central South University  Haikou China"},{"name":"Department of Neurosurgery The First Affiliated Hospital of Hainan University  Haikou 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