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@ARTICLE{Shrouder:268500,
      author       = {Shrouder, Joshua James and Calandra, Gian-Marco and Filser,
                      Severin and Varga, Daniel Peter and Besson-Girard, Simon and
                      Mamrak, Uta and Dorok, Maximilian and Bulut-Impraim, Buket
                      and Seker, Fatma Burcu and Gesierich, Benno and Laredo,
                      Fabio and Wehn, Antonia Clarissa and Khalin, Igor and Bayer,
                      Patrick and Liesz, Arthur and Gökce, Ozgun and Plesnila,
                      Nikolaus},
      title        = {{C}ontinued dysfunction of capillary pericytes promotes
                      no-reflow after experimental stroke in vivo.},
      journal      = {Brain},
      volume       = {147},
      number       = {3},
      issn         = {0006-8950},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DZNE-2024-00246},
      pages        = {1057 - 1074},
      year         = {2024},
      abstract     = {Incomplete reperfusion of the microvasculature
                      ('no-reflow') after ischaemic stroke damages salvageable
                      brain tissue. Previous ex vivo studies suggest pericytes are
                      vulnerable to ischaemia and may exacerbate no-reflow, but
                      the viability of pericytes and their association with
                      no-reflow remains under-explored in vivo. Using longitudinal
                      in vivo two-photon single-cell imaging over 7 days, we
                      showed that $87\%$ of pericytes constrict during cerebral
                      ischaemia and remain constricted post reperfusion, and
                      $50\%$ of the pericyte population are acutely damaged.
                      Moreover, we revealed ischaemic pericytes to be
                      fundamentally implicated in capillary no-reflow by limiting
                      and arresting blood flow within the first 24 h post stroke.
                      Despite sustaining acute membrane damage, we observed that
                      over half of all cortical pericytes survived ischaemia and
                      responded to vasoactive stimuli, upregulated unique
                      transcriptomic profiles and replicated. Finally, we
                      demonstrated the delayed recovery of capillary diameter by
                      ischaemic pericytes after reperfusion predicted vessel
                      reconstriction in the subacute phase of stroke.
                      Cumulatively, these findings demonstrate that surviving
                      cortical pericytes remain both viable and promising
                      therapeutic targets to counteract no-reflow after ischaemic
                      stroke.},
      keywords     = {Humans / Stroke / Pericytes: physiology / Brain Ischemia /
                      Ischemic Stroke / Cerebral Infarction / cerebral ischaemia
                      (Other) / ischaemic stroke (Other) / no-reflow (Other) /
                      pericytes (Other) / reperfusion (Other)},
      cin          = {LMF},
      ddc          = {610},
      cid          = {I:(DE-2719)1040180},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38153327},
      doi          = {10.1093/brain/awad401},
      url          = {https://pub.dzne.de/record/268500},
}