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@ARTICLE{Yin:284045,
      author       = {Yin, Yue and Li, Zixuan and Shu, Weijie and Liu, Hening and
                      Wang, Zihan and Fu, Cong and Zhu, Yuanbo and Li, Xuejing and
                      Zhang, Yi and Lv, Bei and Wang, Zixuan and Zhao, Qiaoqiao
                      and Liu, Dan and Tang, Lu and Wang, Wei},
      title        = {{I}ntranasal blood-brain barrier bypass enables sequential
                      mitochondria-targeted bioengineered nanolamellar system for
                      ischemic stroke therapy.},
      journal      = {Nature Communications},
      volume       = {17},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2026-00080},
      pages        = {760},
      year         = {2026},
      abstract     = {Mitochondrial damage constitutes the central pathological
                      mechanism of cerebral ischemia-reperfusion (I/R) injury.
                      Targeted delivery of antioxidants to mitochondria and the
                      phenotype polarization of glial cells holds great promise
                      for effective treatment. However, the blood-brain barrier
                      (BBB) remains a major obstacle, causing insufficient drug
                      accumulation in neuronal mitochondria. Here, we develop a
                      bioengineered nanolamellar system (MM@BPPF) by coating
                      microglia-mitochondria hybrid biomembrane onto black
                      phosphorus nanosheets (BP NSs) loaded with polymetformin
                      (PolyMet) and fingolimod hydrochloride (FTY720). Microglia
                      membrane facilitates inflammation-directed targeting to the
                      injured brain regions, while mitochondria membrane confers
                      homotypic targeting to mitochondria. Meanwhile, BP NSs,
                      PolyMet, and FTY720 act sequentially to restore
                      mitochondrial function of neuronal cells and modulate
                      microglial polarization. Intranasal administration enables
                      MM@BPPF to bypass the BBB, substantially improving
                      brain-targeting efficiency. This work not only offers an
                      innovative sequential targeting strategy for mitigating I/R
                      injury but also presents a potential paradigm for treating
                      other central nervous system disorders.},
      keywords     = {Blood-Brain Barrier: metabolism / Blood-Brain Barrier: drug
                      effects / Animals / Mitochondria: metabolism / Mitochondria:
                      drug effects / Microglia: metabolism / Microglia: drug
                      effects / Mice / Ischemic Stroke: drug therapy / Ischemic
                      Stroke: metabolism / Ischemic Stroke: pathology /
                      Administration, Intranasal / Fingolimod Hydrochloride:
                      administration $\&$ dosage / Fingolimod Hydrochloride:
                      pharmacology / Reperfusion Injury: drug therapy / Male /
                      Mice, Inbred C57BL / Drug Delivery Systems: methods /
                      Bioengineering / Neurons: drug effects / Neurons: metabolism
                      / Disease Models, Animal / Brain: metabolism / Brain: drug
                      effects / Fingolimod Hydrochloride (NLM Chemicals)},
      cin          = {AG Liu},
      ddc          = {500},
      cid          = {I:(DE-2719)1012009},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41547891},
      doi          = {10.1038/s41467-025-68024-5},
      url          = {https://pub.dzne.de/record/284045},
}