Molecular Mechanisms of Cardiac Remodeling and Regeneration in Physical Exercise

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 cardiomyo...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2019-09, Vol.8 (10), p.1128
Main Authors: Schüttler, Dominik, Clauss, Sebastian, Weckbach, Ludwig T, Brunner, Stefan
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
Aging
AKT protein
Akt signaling
Angina pectoris
Animal models
cardiac cellular regeneration
Cardiac function
cardiac hypertrophy
cardiomyocyte proliferation
Cardiomyocytes
cardioprotection
Cardiovascular diseases
Cardiovascular system
Cell growth
Congestive heart failure
Coronary artery disease
Exercise
Gene expression
Heart failure
Hypertension
Hypertrophy
Injuries
Intracellular
Intracellular signalling
Ischemia
Kinases
Mammals
Metabolism
microRNA (miR)
miRNA
Mitochondria
Molecular modelling
Nitric oxide
Phenotypes
Physical activity
physical exercise
Physical fitness
Physical training
Physiology
Progenitor cells
Proteins
Rapamycin
Review
Stem cells
Therapeutic targets
TOR protein
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Summary: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.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells8101128