PMID- 31547508
OWN - NLM
STAT- MEDLINE
DCOM- 20200615
LR  - 20200615
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 8
IP  - 10
DP  - 2019 Sep 23
TI  - Molecular Mechanisms of Cardiac Remodeling and Regeneration in Physical Exercise.
LID - 10.3390/cells8101128 [doi]
LID - 1128
AB  - Regular physical activity with aerobic and muscle-strengthening training protects 
      against the occurrence and progression of cardiovascular disease and can improve 
      cardiac function in heart failure patients. In the past decade significant 
      advances have been made in identifying mechanisms of cardiomyocyte re-programming 
      and renewal including an enhanced exercise-induced proliferational capacity of 
      cardiomyocytes and its progenitor cells. Various intracellular mechanisms 
      mediating these positive effects on cardiac function have been found in animal 
      models of exercise and will be highlighted in this review. 1) activation of 
      extracellular and intracellular signaling pathways including phosphatidylinositol 
      3 phosphate kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin 
      (mTOR), EGFR/JNK/SP-1, nitric oxide (NO)-signaling, and extracellular vesicles; 
      2) gene expression modulation via microRNAs (miR), in particular via miR-17-3p 
      and miR-222; and 3) modulation of cardiac cellular metabolism and mitochondrial 
      adaption. Understanding the cellular mechanisms, which generate an 
      exercise-induced cardioprotective cellular phenotype with physiological 
      hypertrophy and enhanced proliferational capacity may give rise to novel 
      therapeutic targets. These may open up innovative strategies to preserve cardiac 
      function after myocardial injury as well as in aged cardiac tissue.
FAU - Schuttler, Dominik
AU  - Schuttler D
AD  - Department of Medicine I, University Hospital Munich, Campus Grosshadern and 
      Innenstadt, Ludwig-Maximilians University Munich (LMU), 81377 Munich, Germany. 
      Dominik.Schuettler@med.uni-muenchen.de.
AD  - DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Munich 
      Heart Alliance (MHA), 80336 Munich, Germany. 
      Dominik.Schuettler@med.uni-muenchen.de.
AD  - Walter Brendel Centre of Experimental Medicine, Ludwig-Maximilians University 
      Munich (LMU), 81377 Munich, Germany. Dominik.Schuettler@med.uni-muenchen.de.
FAU - Clauss, Sebastian
AU  - Clauss S
AUID- ORCID: 0000-0002-5675-6128
AD  - Department of Medicine I, University Hospital Munich, Campus Grosshadern and 
      Innenstadt, Ludwig-Maximilians University Munich (LMU), 81377 Munich, Germany. 
      Sebastian.Clauss@med.uni-muenchen.de.
AD  - DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Munich 
      Heart Alliance (MHA), 80336 Munich, Germany. 
      Sebastian.Clauss@med.uni-muenchen.de.
AD  - Walter Brendel Centre of Experimental Medicine, Ludwig-Maximilians University 
      Munich (LMU), 81377 Munich, Germany. Sebastian.Clauss@med.uni-muenchen.de.
FAU - Weckbach, Ludwig T
AU  - Weckbach LT
AD  - Department of Medicine I, University Hospital Munich, Campus Grosshadern and 
      Innenstadt, Ludwig-Maximilians University Munich (LMU), 81377 Munich, Germany. 
      Ludwig.Wekcbach@med.uni-muenchen.de.
AD  - DZHK (German Centre for Cardiovascular Research), Partner Site Munich, Munich 
      Heart Alliance (MHA), 80336 Munich, Germany. Ludwig.Wekcbach@med.uni-muenchen.de.
AD  - Walter Brendel Centre of Experimental Medicine, Ludwig-Maximilians University 
      Munich (LMU), 81377 Munich, Germany. Ludwig.Wekcbach@med.uni-muenchen.de.
AD  - Institute of Cardiovascular Physiology and Pathophysiology, Biomedical Center, 
      Ludwig-Maximilians-University Munich, 82152 Planegg-Martinsried, Germany. 
      Ludwig.Wekcbach@med.uni-muenchen.de.
FAU - Brunner, Stefan
AU  - Brunner S
AD  - Department of Medicine I, University Hospital Munich, Campus Grosshadern and 
      Innenstadt, Ludwig-Maximilians University Munich (LMU), 81377 Munich, Germany. 
      stefan.brunner@med.uni-muenchen.de.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190923
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
SB  - IM
MH  - Animals
MH  - Exercise/*physiology
MH  - Heart/*physiology/physiopathology
MH  - Humans
MH  - Myocytes, Cardiac/physiology
MH  - Regeneration/*physiology
MH  - Signal Transduction/genetics
MH  - Ventricular Remodeling/*physiology
PMC - PMC6829258
OTO - NOTNLM
OT  - Akt signaling
OT  - cardiac cellular regeneration
OT  - cardiac hypertrophy
OT  - cardiomyocyte proliferation
OT  - cardioprotection
OT  - microRNA (miR)
OT  - physical exercise
COIS- The authors declare there are no conflicts of interest.
EDAT- 2019/09/25 06:00
MHDA- 2020/06/17 06:00
PMCR- 2019/10/01
CRDT- 2019/09/25 06:00
PHST- 2019/09/02 00:00 [received]
PHST- 2019/09/19 00:00 [revised]
PHST- 2019/09/19 00:00 [accepted]
PHST- 2019/09/25 06:00 [entrez]
PHST- 2019/09/25 06:00 [pubmed]
PHST- 2020/06/17 06:00 [medline]
PHST- 2019/10/01 00:00 [pmc-release]
AID - cells8101128 [pii]
AID - cells-08-01128 [pii]
AID - 10.3390/cells8101128 [doi]
PST - epublish
SO  - Cells. 2019 Sep 23;8(10):1128. doi: 10.3390/cells8101128.