The Athlete's Heart vs. the Failing Heart: Can Signaling Explain the Two Distinct Outcomes?

Weeks, Kate L.; McMullen, Julie R.

doi:10.1152/physiol.00043.2010

Cited by 140 publications

(127 citation statements)

References 111 publications

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“…Akt1 is phosphorylated in physiological cardiac hypertrophy and exerts diverse beneficial functions such as inhibition of cardiomyocyte apoptosis, improvement in calcium transients, and cardiac hypertrophy (46,62). A series of studies led by the McMullen's group (63,64,98) has shown the role of insulin-like growth factor 1 (IGF-1)/IGF-1 receptor (IGF-1R)/PI3K (110␣) in the development of physiological cardiac hypertrophy. *Predicted target gene.…”

Section: Mirnas Cardiac Hypertrophy and Exercise Trainingmentioning

confidence: 99%

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

Fernandes

Baraúna

Negräo

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

126

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Fernandes T, Baraúna VG, Negrão CE, Phillips MI, Oliveira EM. Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs. Am J Physiol Heart Circ Physiol 309: H543-H552, 2015. First published June 12, 2015 doi:10.1152/ajpheart.00899.2014 hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic exercise induces beneficial physiological LV remodeling. The molecular/cellular mechanisms for this effect are not totally known, and here we review various mechanisms including the role of microRNA (miRNA). Studies in the heart, have identified antihypertrophic . Four miRNAs are recognized as cardiacspecific: miRNA-1, -133a/b, -208a/b, and -499 and called myomiRs. In our studies we have shown that miRNAs respond to swimming aerobic exercise by 1) decreasing cardiac fibrosis through miRNA-29 increasing and inhibiting collagen, 2) increasing angiogenesis through miRNA-126 by inhibiting negative regulators of the VEGF pathway, and 3) modulating the renin-angiotensin system through the miRNAs-27a/b and -143. Exercise training also increases cardiomyocyte growth and survival by swimming-regulated miRNA-1, -21, -27a/b, -29a/c, -30e, -99b, -100, -124, -126, -133a/b, -143, -144, -145, -208a, and -222 and running-regulated miRNA-1, -26, -27a, -133, -143, -150, and -222, which influence genes associated with the heart remodeling and angiogenesis. We conclude that there is a potential role of these miRNAs in promoting cardioprotective effects on physiological growth. cardiac hypertrophy; angiogenesis; swimming training; running training; microRNA THIS ARTICLE is part of a collection on Exercise Training in Cardiovascular Disease: Cell, Molecular, and Integrative Perspectives. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology.org/.EXERCISE TRAINING IS the most effective nonpharmacological intervention to reduce cardiovascular disease (CVD). Its prescription is recommended by the guidelines of the most important entities, such as the American College of Sport Medicine and the American Heart Association (39).Exercise training is well known to promote beneficial adaptations in the cardiovascular system which can vary according to type, intensity, and duration of exercise (32). Exercise training induces marked beneficial systemic effects on metabolism control, skeletal muscle, cognitive function, and cardiovascular function (30, 39). Among them, the set of adaptations induced in the myocardium are collectively referred to as "athlete's heart" and includes increased cardiac mass, formations of new blood vessels, and decreased collagen content (15a, 17, 20, 23, 77, 91). Individuals with high levels of physical activity have a lower prevalence and lower death rates from CVD (32, 86). Thus exercise training has been established not only as a way to ma...

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Section: Mirnas Cardiac Hypertrophy and Exercise Trainingmentioning

confidence: 99%

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

Fernandes

Baraúna

Negräo

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

126

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“…The adult heart can adapt to stress by hypertrophy and vascular growth/remodeling (Bernardo et al, 2010;Weeks KL and McMullen JR, 2011). Physiological or adaptive responses, as in the case of the exercised trained athelete's heart, are characterized by balanced changes in both the cardiomyocytes and the vasculature.…”

Section: Regulating the Coronary Vessels Within The Adult Heart For Cmentioning

confidence: 99%

“…The physiological and pathological responses overlap in some respects, especially in the early stages of adaptation. However, there are distinct characteristics to the physiological and pathological responses that have been revealed by studies in humans and rodent models (Boström P et al, 2010;Pavlik G et al, 2010;Weeks KL and McMullen JR, 2011). These differences include the degree of vascularization of the myocardium with the physiological response leading to increased vascularization.…”

Section: Regulating the Coronary Vessels Within The Adult Heart For Cmentioning

confidence: 99%

Cardiac Vasculature: Development and Pathology

Watanabe¹,

Wikenheiser²,

Ramírez-Bergeron³

et al. 2011

Vasculogenesis and Angiogenesis - From Embryonic Development to Regenerative Medicine

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“…Increased workload, such as during exercise or chronic disease stresses causing pressure overload, induces cardiomyocyte hypertrophy, while hemodynamic unloading leads to heart atrophy (1)(2)(3). Such changes in cell size depend on the equilibrium between the rates of protein synthesis and degradation, both of which are finely regulated by a number of signaling pathways and require a tight control over protein turnover and protein quality control to avoid accumulation of unfolded/ misfolded proteins and subsequent ER stress (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Atrogin-1 deficiency promotes cardiomyopathy and premature death via impaired autophagy

et al. 2014

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Cardiomyocyte proteostasis is mediated by the ubiquitin/proteasome system (UPS) and autophagy/lysosome system and is fundamental for cardiac adaptation to both physiologic (e.g., exercise) and pathologic (e.g., pressure overload) stresses. Both the UPS and autophagy/lysosome system exhibit reduced efficiency as a consequence of aging, and dysfunction in these systems is associated with cardiomyopathies. The musclespecific ubiquitin ligase atrogin-1 targets signaling proteins involved in cardiac hypertrophy for degradation. Here, using atrogin-1 KO mice in combination with in vivo pulsed stable isotope labeling of amino acids in cell culture proteomics and biochemical and cellular analyses, we identified charged multivesicular body protein 2B (CHMP2B), which is part of an endosomal sorting complex (ESCRT) required for autophagy, as a target of atrogin-1-mediated degradation. Mice lacking atrogin-1 failed to degrade CHMP2B, resulting in autophagy impairment, intracellular protein aggregate accumulation, unfolded protein response activation, and subsequent cardiomyocyte apoptosis, all of which increased progressively with age. Cellular proteostasis alterations resulted in cardiomyopathy characterized by myocardial remodeling with interstitial fibrosis, with reduced diastolic function and arrhythmias. CHMP2B downregulation in atrogin-1 KO mice restored autophagy and decreased proteotoxicity, thereby preventing cell death. These data indicate that atrogin-1 promotes cardiomyocyte health through mediating the interplay between UPS and autophagy/lysosome system and its alteration promotes development of cardiomyopathies.

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The Athlete's Heart vs. the Failing Heart: Can Signaling Explain the Two Distinct Outcomes?

Cited by 140 publications

References 111 publications

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

Cardiac Vasculature: Development and Pathology

Atrogin-1 deficiency promotes cardiomyopathy and premature death via impaired autophagy

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