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@ARTICLE{Stratmann:285480,
      author       = {Stratmann, Maite and Gagliardi, Caterina and Capasso,
                      Melania},
      title        = {{P}roton channel {H}v1 modulates microglial responses to
                      neurological disorders},
      journal      = {Frontiers in biophysics},
      volume       = {3},
      issn         = {2813-7183},
      address      = {Lausanne},
      publisher    = {Frontiers Media SA},
      reportid     = {DZNE-2026-00257},
      pages        = {1681011},
      year         = {2025},
      abstract     = {Proton channels are transmembrane proteins that enable
                      selective proton (H+) transport. The voltage-gated proton
                      channel Hv1 or HVCN1 is the only one found in mammalian
                      cells, primarily in immune cells, where it facilitates rapid
                      proton extrusion in response to membrane depolarization,
                      mediating outward proton currents. Therefore, it is well
                      equipped to support NADPH-oxidase function, facilitating the
                      proton flux that maintains physiological pH and membrane
                      potential for efficient reactive oxygen species (ROS)
                      production. In the central nervous system (CNS), Hv1 is
                      predominantly found in microglia. Its role in microglia
                      homeostasis is yet to be elucidated; however, recent
                      research has highlighted its involvement in neurological
                      conditions, including demyelinating disease, spinal cord
                      injury, stroke, and Parkinsonism. These studies have shown
                      beneficial effects of Hv1 deletion, including improved
                      neurological function, reduced microglial activation,
                      enhanced myelination, and decreased neuroinflammation. This
                      review explores the role of Hv1 in the CNS and its potential
                      as a therapeutic target in neurodegenerative diseases.},
      cin          = {AG Capasso},
      ddc          = {570},
      cid          = {I:(DE-2719)1013033},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.3389/frbis.2025.1681011},
      url          = {https://pub.dzne.de/record/285480},
}