scholarly journals MTOR Signaling-Related MicroRNAs As Cardiac Hypertrophy Modulators In High- Volume Endurance Training

2021 ◽  
Vol 53 (8S) ◽  
pp. 67-67
Author(s):  
Bruno Rocha de Avila Pelozin ◽  
Ursula Paulo Renó Soci ◽  
João Lucas Penteado Gomes ◽  
Edilamar Menezes de Oliveira ◽  
Tiago Fernandes
Keyword(s):  
Cardiac Hypertrophy ◽  
Endurance Training ◽  
High Volume ◽  
Mtor Signaling

scholarly journals KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Wang ◽  
Hongjuan Liao ◽  
Yueheng Wang ◽  
Jinlin Zhou ◽  
Feng Wang ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Mtor Signaling ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Quantitative Real Time Pcr

Abstract Background Cardiovascular diseases have become the leading cause of death worldwide, and cardiac hypertrophy is the core mechanism underlying cardiac defect and heart failure. However, the underlying mechanisms of cardiac hypertrophy are not fully understood. Here we investigated the roles of Kallikrein 11 (KLK11) in cardiac hypertrophy. Methods Human and mouse hypertrophic heart tissues were used to determine the expression of KLK11 with quantitative real-time PCR and western blot. Mouse cardiac hypertrophy was induced by transverse aortic constriction (TAC), and cardiomyocyte hypertrophy was induced by angiotensin II. Cardiac function was analyzed by echocardiography. The signaling pathway was analyzed by western blot. Protein synthesis was monitored by the incorporation of [3H]-leucine. Gene expression was analyzed by quantitative real-time PCR. Results The mRNA and protein levels of KLK11 were upregulated in human hypertrophic hearts. We also induced cardiac hypertrophy in mice and observed the upregulation of KLK11 in hypertrophic hearts. Our in vitro experiments demonstrated that KLK11 overexpression promoted whereas KLK11 knockdown repressed cardiomyocytes hypertrophy induced by angiotensin II, as evidenced by cardiomyocyte size and the expression of hypertrophy-related fetal genes. Besides, we knocked down KLK11 expression in mouse hearts with adeno-associated virus 9. Knockdown of KLK11 in mouse hearts inhibited TAC-induced decline in fraction shortening and ejection fraction, reduced the increase in heart weight, cardiomyocyte size, and expression of hypertrophic fetal genes. We also observed that KLK11 promoted protein synthesis, the key feature of cardiomyocyte hypertrophy, by regulating the pivotal machines S6K1 and 4EBP1. Mechanism study demonstrated that KLK11 promoted the activation of AKT-mTOR signaling to promote S6K1 and 4EBP1 pathway and protein synthesis. Repression of mTOR with rapamycin blocked the effects of KLK11 on S6K1 and 4EBP1 as well as protein synthesis. Besides, rapamycin treatment blocked the roles of KLK11 in the regulation of cardiomyocyte hypertrophy. Conclusions Our findings demonstrated that KLK11 promoted cardiomyocyte hypertrophy by activating AKT-mTOR signaling to promote protein synthesis.

Berberine Attenuates Cardiac Hypertrophy Through Inhibition of mTOR Signaling Pathway

2020 ◽  
Vol 34 (4) ◽  
pp. 463-473
Author(s):  
Xing Chen ◽  
Xingzuan Jiang ◽  
Chuanfang Cheng ◽  
Jing Chen ◽  
Shuyan Huang ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

TIME COURSE OF THE DEVELOPMENT OF CARDIAC HYPERTROPHY WITH ENDURANCE TRAINING

1976 ◽  
Vol 8 (1) ◽  
pp. 55 ◽  
Author(s):  
R. C. Hickson ◽  
G. T. Hammons ◽  
R. K. Conlee ◽  
J. O. Holloszy
Keyword(s):  
Cardiac Hypertrophy ◽  
Endurance Training ◽  
Time Course

Abstract 422: CITED4 is Sufficient to Induce Physiologic Cardiac Hypertrophy and Necessary to Protect Against Pathological Hemodynamic Stress

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Carolin Lerchenmueller ◽  
Vassilios J Bezzeridis ◽  
Colin Platt ◽  
Chunyang Xiao ◽  
Anthony Rosenzweig
Keyword(s):  
Cardiac Hypertrophy ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Ischemia Reperfusion ◽  
Mtor Signaling ◽  
Swimming Exercise ◽  
Heart Weight ◽  
Hemodynamic Stress ◽  
Post Surgery ◽  
Adverse Remodeling

Cardiac hypertrophy is an adaptive response to increased physiologic or pathologic hemodynamic stress. Previous work from our laboratory suggested that the CEBPβ/ CITED4 pathway plays an important role in exercise-induced cardiac hypertrophy. Consistent with this model, our laboratory recently found that inducible cardiac expression of CITED4 in adult mice increases heart weight and cardiomyocyte size with normal systolic function and a gene expression profile consistent with physiologic growth. After ischemia-reperfusion injury (IRI), induced CITED4 mice show significant functional recovery and evidence for decreased adverse remodeling. Next, we sought to investigate the role of CITED4 in the setting of physiologic (forced swimming exercise) and pathological (transverse aortic constriction, TAC) cardiac hypertrophy. Cardiomyocyte-specific CITED4 knockout mice (C4KO) undergoing a three week swimming exercise protocol showed modestly but significantly reduced systolic function when compared to control animals (%FS controls 55.4±1.09 vs. C4KO 51.75±0.86; p=0.025). C4KO mice exposed to TAC demonstrated a more rapid and severe decline in cardiac function after TAC (at 6 weeks post surgery, %FS controls 41.55±2.06 vs. C4KO 32.51±2.67; p=0.024). Both in vitro and in vivo we demonstrate that CITED4 is necessary and sufficient for activation of mTOR signaling. Of note, mTORC1 inhibition by rapamycin abrogated the beneficial effects of CITED4 expression after IRI. Taken together, our data identify CITED4 as a novel regulator of mTOR signaling. Moreover they demonstrate that CITED4 is sufficient for physiologic growth and to protect against adverse remodeling after ischemic injury. CITED4 is also necessary for adaptive responses to pathological biomechanical stress and may represent a novel therapeutic target to mitigate adverse ventricular remodeling.

mTOR signaling-related microRNAs as cardiac hypertrophy modulators in high‐volume endurance training

2021 ◽  
Author(s):  
Bruno R.A. Pelozin ◽  
Ursula Paula Reno Soci ◽  
João L. P. Gomes ◽  
Edilamar Menezes Oliveira ◽  
Tiago Fernandes
Keyword(s):  
Protein Expression ◽  
Molecular Mechanisms ◽  
High Volume ◽  
Left Ventricular ◽  
Mtor Signaling ◽  
Neonatal Rat ◽  
Cardiomyocyte Hypertrophy ◽  
Peak Exercise ◽  
Dependent Manner ◽  
Rat Cardiomyocytes

Aerobic exercise training (ET) promotes cardiovascular adaptations, including physiological left ventricular hypertrophy (LVH). However, the molecular mechanisms that underlying these changes are unclear. The study aimed to elucidate specific miRNAs and target genes involved with the Akt/mTOR signaling in high-volume ET-induced LVH. Eight-week-old female Wistar rats were assigned to three groups: sedentary control (SC), trained protocol 1 (P1), and trained protocol 2 (P2). P1 consisted of 60 minutes/day of swimming, 5x/week, for 10 weeks. P2 consisted of the same protocol as P1 until the 8th week; in the 9th week, rats trained 2x/day, and in the 10th week, trained 3x/day. Subsequently, structure and molecular parameters were evaluated in the heart. Trained groups demonstrate higher values to VO2 peak, exercise tolerance, and LVH in a volume-dependent manner. The miRNA-26a-5p levels were higher in P1 and P2 compared to SC group (150±15%, d=1.8; 148±16%, d=1.7; and 100±7%, respectively, P < 0.05). In contrast, miRNA-16-5p levels were lower in P1 and P2 compared to SC group (69±5%, d=2.3, P < 0.01; 37±4%, d=5.6, P < 0.001 and 100±6%, respectively). Additionally, miRNA-16-5p knockdown and miRNA-26a-5p overexpression significantly promoted cardiomyocyte hypertrophy in neonatal rat cardiomyocytes. Both miRNAs were selected, using Diana Tolls bioinformatics website, for acting in the mTOR signaling pathway. The protein expression of Akt, mTOR, p70S6k, and 4E-BP1 were greater in P1 and even more pronounced in P2. Nonetheless, GSK3β protein expression was lower in trained groups. Together, these molecular changes may contribute to a pronounced physiological LVH observed in high-volume aerobic training.

scholarly journals β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice

Life ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 357
Author(s):  
Volodymyr V. Balatskyi ◽  
Oksana L. Palchevska ◽  
Lina Bortnichuk ◽  
Ana-Maria Gan ◽  
Anna Myronova ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cardiac Hypertrophy ◽  
Endurance Training ◽  
Metabolic Regulation ◽  
Training Model ◽  
Cardiac Metabolism ◽  
Mitogen Activated Protein Kinase ◽  
Hypertrophic Growth ◽  
Physiological Cardiac Hypertrophy ◽  
Mitogen Activated Protein

The role of canonical Wnt signaling in metabolic regulation and development of physiological cardiac hypertrophy remains largely unknown. To explore the function of β-catenin in the regulation of cardiac metabolism and physiological cardiac hypertrophy development, we used mice heterozygous for cardiac-specific β-catenin knockout that were subjected to a swimming training model. β-Catenin haploinsufficient mice subjected to endurance training displayed a decreased β-catenin transcriptional activity, attenuated cardiomyocytes hypertrophic growth, and enhanced activation of AMP-activated protein kinase (AMPK), phosphoinositide-3-kinase–Akt (Pi3K–Akt), and mitogen-activated protein kinase/extracellular signal-regulated kinases 1/2 (MAPK/Erk1/2) signaling pathways compared to trained wild type mice. We further observed an increased level of proteins involved in glucose aerobic metabolism and β-oxidation along with perturbed activity of mitochondrial oxidative phosphorylation complexes (OXPHOS) in trained β-catenin haploinsufficient mice. Taken together, Wnt/β-catenin signaling appears to govern metabolic regulatory programs, sustaining metabolic plasticity in adult hearts during the adaptation to endurance training.

scholarly journals A Brief Review on Concurrent Training: From Laboratory to the Field

Sports ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 127 ◽  
Author(s):  
Spyridon Methenitis
Keyword(s):  
Protein Kinase ◽  
Endurance Training ◽  
Mammalian Target Of Rapamycin ◽  
Interval Training ◽  
Adenosine Monophosphate ◽  
High Volume ◽  
Concurrent Training ◽  
Peroxisome Proliferator ◽  
Negative Effects ◽  
Peroxisome Proliferator Activated Receptor

The majority of sports rely on concurrent training (CT; e.g., the simultaneous training of strength and endurance). However, a phenomenon called “Concurrent training effect” (CTE), which is a compromise in adaptation resulting from concurrent training, appears to be mostly affected by the interference of the molecular pathways of the underlying adaptations from each type of training segments. Until now, it seems that the volume, intensity, type, frequency of endurance training, as well as the training history and background strongly affect the CTE. High volume, moderate, continuous and frequent endurance training, are thought to negatively affect the resistance training-induced adaptations, probably by inhibition of the Protein kinase B—mammalian target of rapamycin pathway activation, of the adenosine monophosphate-activated protein kinase (AMPK). In contrast, it seems that short bouts of high-intensity interval training (HIIT) or sprint interval training (SIT) minimize the negative effects of concurrent training. This is particularly the case when HIIT and SIT incorporated in cycling have even lower or even no negative effects, while they provide at least the same metabolic adaptations, probably through the peroxisome proliferator-activated receptor-γ coactivator (PGC-1a) pathway. However, significant questions about the molecular events underlying the CTE remain unanswered.

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