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@ARTICLE{vanPutten:892867,
      author       = {van Putten, Michel J. A. M. and Fahlke, Christoph and
                      Kafitz, Karl W. and Hofmeijer, Jeannette and Rose, Christine
                      R.},
      title        = {{D}ysregulation of {A}strocyte {I}on {H}omeostasis and
                      {I}ts {R}elevance for {S}troke-{I}nduced {B}rain {D}amage},
      journal      = {International journal of molecular sciences},
      volume       = {22},
      number       = {11},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {FZJ-2021-02406},
      pages        = {5679 -},
      year         = {2021},
      abstract     = {Ischemic stroke is a leading cause of mortality and chronic
                      disability. Either recovery or progression towards
                      irreversible failure of neurons and astrocytes occurs within
                      minutes to days, depending on remaining perfusion levels.
                      Initial damage arises from energy depletion resulting in a
                      failure to maintain homeostasis and ion gradients between
                      extra- and intracellular spaces. Astrocytes play a key role
                      in these processes and are thus central players in the
                      dynamics towards recovery or progression of stroke-induced
                      brain damage. Here, we present a synopsis of the pivotal
                      functions of astrocytes at the tripartite synapse, which
                      form the basis of physiological brain functioning. We
                      summarize the evidence of astrocytic failure and its
                      consequences under ischemic conditions. Special emphasis is
                      put on the homeostasis and stroke-induced dysregulation of
                      the major monovalent ions, namely Na+, K+, H+, and Cl-, and
                      their involvement in maintenance of cellular volume and
                      generation of cerebral edema.},
      cin          = {IBI-1},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IBI-1-20200312},
      pnm          = {524 - Molecular and Cellular Information Processing
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-524},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34073593},
      UT           = {WOS:000660219900001},
      doi          = {10.3390/ijms22115679},
      url          = {https://juser.fz-juelich.de/record/892867},
}