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@ARTICLE{Veltkamp:141325,
      author       = {R. Veltkamp and S. Uhlmann and M. Marinescu and C. Sticht
                      and D. Finke and N. Gretz and H.-J. Gröne$^*$ and H. A.
                      Katus and J. Backs and L. H. Lehmann},
      title        = {{E}xperimental ischaemic stroke induces transient cardiac
                      atrophy and dysfunction.},
      journal      = {Journal of cachexia, sarcopenia and muscle},
      volume       = {10},
      number       = {1},
      issn         = {2190-5991},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DKFZ-2018-01844},
      pages        = {54-62},
      year         = {2019},
      abstract     = {Stroke can lead to cardiac dysfunction in patients, but the
                      mechanisms underlying the interaction between the injured
                      brain and the heart are poorly understood. The objective of
                      the study is to investigate the effects of experimental
                      murine stroke on cardiac function and molecular signalling
                      in the heart.Mice were subjected to filament-induced left
                      middle cerebral artery occlusion for 30 or 60 min or sham
                      surgery and underwent repetitive micro-echocardiography.
                      Left ventricular contractility was reduced early (24-72 h)
                      but not late (2 months) after brain ischaemia. Cardiac
                      dysfunction was accompanied by a release of high-sensitive
                      cardiac troponin (hsTNT (ng/ml): d1: 7.0 ± 1.0 vs.
                      25.0 ± 3.2*; d3: 7.3 ± 1.1 vs. 52.2 ± 16.7*;
                      d14: 5.7 ± 0.8 vs. 5.2 ± 0.3; sham vs. 60 min.
                      MCAO; mean ± SEM; *p < 0.05); reduced heart weight
                      (heart weight/tibia length ratio: d1: 6.9 ± 0.2 vs.
                      6.4 ± 0.1*; d3: 6.7 ± 0.2 vs. 5.8 ± 0.1*;
                      d14: 6.7 ± 0.2 vs. 6.4 ± 03; sham vs. 60 min.
                      MCAO; mean ± SEM; *p < 0.05); resulting from
                      cardiomyocyte atrophy (cardiomyocyte size: d1:
                      $12.8\% ± 0.002**;$ d3: $13.5\% ± 0.002**;$ 14d:
                      $6.3\% ± 0.003*;$ 60 min. MCAO vs. sham;
                      mean ± SEM; **p < 0.01; *p < 0.05), accompanied
                      by increased atrogin-1 and the E3 ubiquitin ligase murf-1.
                      Net norepinephrine but not synthesis was increased,
                      suggesting a reduced norepinephrine release or an increase
                      of norepinephrine re-uptake, resulting in a functional
                      denervation. Transcriptome analysis in cardiac tissue
                      identified the transcription factor peroxisome
                      proliferator-activated receptor gamma as a potential
                      mediator of stroke-induced transcriptional dysregulation
                      involved in cardiac atrophy.Stroke induces a complex
                      molecular response in the heart muscle with immediate but
                      transient cardiac atrophy and dysfunction.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {322 - Genetics and Pathophysiology (POF3-322)},
      pid          = {G:(DE-HGF)POF3-322},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30378296},
      doi          = {10.1002/jcsm.12335},
      url          = {https://inrepo02.dkfz.de/record/141325},
}