{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T21:28:51Z","timestamp":1789939731930,"version":"4.0.1"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2018,10,30]],"date-time":"2018-10-30T00:00:00Z","timestamp":1540857600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>Mice were subjected to filament\u2010induced left middle cerebral artery occlusion for 30 or 60\u00a0min or sham surgery and underwent repetitive micro\u2010echocardiography. Left ventricular contractility was reduced early (24\u201372\u00a0h) but not late (2\u00a0months) after brain ischaemia. Cardiac dysfunction was accompanied by a release of high\u2010sensitive cardiac troponin (hsTNT (ng\/ml): d1: 7.0\u2009\u00b1\u20091.0 vs. 25.0\u2009\u00b1\u20093.2*; d3: 7.3\u2009\u00b1\u20091.1 vs. 52.2\u2009\u00b1\u200916.7*; d14: 5.7\u2009\u00b1\u20090.8 vs. 5.2\u2009\u00b1\u20090.3; sham vs. 60 min. MCAO; mean \u00b1 SEM; *<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05); reduced heart weight (heart weight\/tibia length ratio: d1: 6.9\u2009\u00b1\u20090.2 vs. 6.4\u2009\u00b1\u20090.1*; d3: 6.7\u2009\u00b1\u20090.2 vs. 5.8\u2009\u00b1\u20090.1*; d14: 6.7\u2009\u00b1\u20090.2 vs. 6.4\u2009\u00b1\u200903; sham vs. 60 min. MCAO; mean \u00b1 SEM; *<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05); resulting from cardiomyocyte atrophy (cardiomyocyte size: d1: 12.8%\u2009\u00b1\u20090.002**; d3: 13.5%\u2009\u00b1\u20090.002**; 14d: 6.3%\u2009\u00b1\u20090.003*; 60 min. MCAO vs. sham; mean\u2009\u00b1\u2009SEM; **<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01; *<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), accompanied by increased atrogin\u20101 and the E3 ubiquitin ligase murf\u20101. Net norepinephrine but not synthesis was increased, suggesting a reduced norepinephrine release or an increase of norepinephrine re\u2010uptake, resulting in a functional denervation. Transcriptome analysis in cardiac tissue identified the transcription factor peroxisome proliferator\u2010activated receptor gamma as a potential mediator of stroke\u2010induced transcriptional dysregulation involved in cardiac atrophy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Stroke induces a complex molecular response in the heart muscle with immediate but transient cardiac atrophy and dysfunction.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12335","type":"journal-article","created":{"date-parts":[[2018,10,31]],"date-time":"2018-10-31T04:14:30Z","timestamp":1540959270000},"page":"54-62","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction"],"prefix":"10.1002","volume":"10","author":[{"given":"Roland","family":"Veltkamp","sequence":"first","affiliation":[{"name":"Division of Brain Sciences Imperial 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