scholarly journals Bioinformatics Analysis Reveals MicroRNAs Regulating Biological Pathways in Exercise-Induced Cardiac Physiological Hypertrophy

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Jiahong Xu ◽  
Yang Liu ◽  
Yuan Xie ◽  
Cuimei Zhao ◽  
Hongbao Wang
Keyword(s):  
Cardiac Hypertrophy ◽  
Target Genes ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Biological Pathways ◽  
Receptor Interaction ◽  
Ventricular Cardiomyopathy ◽  
Functional Annotations ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced ◽  
Physiological Hypertrophy

Exercise-induced physiological cardiac hypertrophy is generally considered to be a type of adaptive change after exercise training and is beneficial for cardiovascular diseases. This study aims at investigating exercise-regulated microRNAs (miRNAs) and their potential biological pathways. Here, we collected 23 miRNAs from 8 published studies. MirPath v.3 from the DIANA tools website was used to execute the analysis, and TargetScan was used to predict the target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to identify potential pathways and functional annotations associated with exercise-induced physiological cardiac hypertrophy. Various miRNA targets and molecular pathways, such as Fatty acid elongation, Arrhythmogenic right ventricular cardiomyopathy (ARVC), and ECM-receptor interaction, were identified. This study could prompt the understanding of the regulatory mechanisms underlying exercise-induced physiological cardiac hypertrophy.

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K

2021 ◽  
Author(s):  
Kate L. Weeks ◽  
Yow Keat Tham ◽  
Suzan G. Yildiz ◽  
Yonali Alexander ◽  
Daniel G. Donner ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Interstitial Fibrosis ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced ◽  
Physiological Hypertrophy ◽  
Constitutively Active

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110a (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy, and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor which regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1) swim training, or 2) cardiac-specific transgenic expression of constitutively active PI3K (caPI3KTg+). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (~21%) in heart weight normalized to tibia length vs untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression, but was comparable between genotypes. However, differences in Foxo3a, Hsp70 and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3KTg+ mice. Cardiac Akt and FoxO1 protein expression were significantly reduced in hearts of caPI3KTg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when considering FoxO1 as a target for treating the diseased heart.

Overexpression of coupling factor 6 attenuates exercise-induced physiological cardiac hypertrophy by inhibiting PI3K/Akt signaling in mice

2012 ◽  
Vol 30 (4) ◽  
pp. 778-786 ◽  
Author(s):  
Shigeki Sagara ◽  
Tomohiro Osanai ◽  
Taihei Itoh ◽  
Kei Izumiyama ◽  
Shuji Shibutani ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Coupling Factor ◽  
Akt Signaling ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced ◽  
Coupling Factor 6

scholarly journals Arrhythmogenic Right Ventricular Cardiomyopathy as a Cause of Palpitations and Syncope in an Otherwise Healthy Active Duty Female

2020 ◽  
Vol 185 (11-12) ◽  
pp. e2173-e2175
Author(s):  
John Blickle ◽  
Ramesh Venkataraman ◽  
Robert D McLeroy
Keyword(s):  
Right Ventricular ◽  
Task Force ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Active Duty ◽  
Exercise Intolerance ◽  
Resonance Imaging ◽  
Ventricular Cardiomyopathy ◽  
Military Population ◽  
Female Soldier ◽  
Exercise Induced

ABSTRACT Identifying the cause of palpitations and syncope in the healthy, active duty military population is important. Most often, the causes are benign, but more malignant etiologies should not be overlooked. In this case, we present a 22-year-old active duty female soldier who developed exercise intolerance, palpitations, and ultimately one episode of exercise-induced syncope. Outpatient evaluation with Holter monitor revealed sustained ventricular tachycardia while exercising. Electrocardiogram revealed findings concerning for arrhythmogenic right ventricular cardiomyopathy based on the 2010 Revised Task Force Criteria. Further investigation with cardiac magnetic resonance imaging helped confirm the diagnosis. Sotalol was used as an antiarrhythmic therapy and an automatic implantable cardioverter defibrillator was implanted to reduce the risk of sudden cardiac death. This case represents an uncommon cause of palpitations and syncope. Arrhythmogenic right ventricular cardiomyopathy should be on the differential diagnosis in the active duty population who present with exercise-induced syncope.

Primary prevention of sudden cardiac death in arrhythmogenic right ventricular cardiomyopathy

ESC CardioMed ◽  
2018 ◽  
pp. 2354-2358
Author(s):  
Katja Zeppenfeld ◽  
Sebastiaan R. D. Piers
Keyword(s):  
Primary Prevention ◽  
Sudden Cardiac Death ◽  
Right Ventricular ◽  
Psychological Health ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Ventricular Cardiomyopathy ◽  
Inherited Cardiomyopathy ◽  
Exercise Induced

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy characterized by progressive fibrofatty replacement of the myocardium, providing the substrate for ventricular reentrant tachycardia, typical for the overt phase of ARVC. Importantly, life-threatening ventricular arrhythmias may also occur in the concealed phase of the disease. The reported rates for sustained ventricular arrhythmias and all-cause mortality in ARVC differ substantially across cohorts. Survival free from sustained ventricular arrhythmias in patients with ARVC-related pathogenic mutations is approximately 66% and 42% at age 40 and 60 years, respectively, in tertiary referral centres. Participation in competitive sports has been associated with an increased propensity of ventricular arrhythmias/death and should therefore be avoided. Beta-blocker therapy may prevent exercise-induced ventricular arrhythmias and should be considered in all patients with ARVC. In patients with unexplained syncope and other recognized risk factors, the implantation of an implantable cardioverter defibrillator (ICD) for primary prevention may be considered. Decisions should be made carefully, weighing the risk of sudden cardiac death, the lifelong risk of complications, and the impact of an ICD on lifestyle and psychological health. ICDs are associated with significant adverse event rates, in particular in young patients who may carry an ICD for several decades.

scholarly journals Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy

2017 ◽  
Vol 242 (18) ◽  
pp. 1820-1830 ◽  
Author(s):  
Stephen W Luckey ◽  
Chris D Haines ◽  
John P Konhilas ◽  
Elizabeth D Luczak ◽  
Antke Messmer-Kratzsch ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Function ◽  
Signaling Pathways ◽  
Mouse Models ◽  
Cyclin D2 ◽  
Cardiac Growth ◽  
Hypertrophic Signaling ◽  
Exercise Induced ◽  
Physiological Hypertrophy ◽  
Mouse Lines

A number of signaling pathways underlying pathological cardiac hypertrophy have been identified. However, few studies have probed the functional significance of these signaling pathways in the context of exercise or physiological pathways. Exercise studies were performed on females from six different genetic mouse models that have been shown to exhibit alterations in pathological cardiac adaptation and hypertrophy. These include mice expressing constitutively active glycogen synthase kinase-3β (GSK-3βS9A), an inhibitor of CaMK II (AC3-I), both GSK-3βS9A and AC3-I (GSK-3βS9A/AC3-I), constitutively active Akt (myrAkt), mice deficient in MAPK/ERK kinase kinase-1 (MEKK1−/−), and mice deficient in cyclin D2 (cyclin D2−/−). Voluntary wheel running performance was similar to NTG littermates for five of the mouse lines. Exercise induced significant cardiac growth in all mouse models except the cyclin D2−/− mice. Cardiac function was not impacted in the cyclin D2−/− mice and studies using a phospho-antibody array identified six proteins with increased phosphorylation (greater than 150%) and nine proteins with decreased phosphorylation (greater than 33% decrease) in the hearts of exercised cyclin D2−/− mice compared to exercised NTG littermate controls. Our results demonstrate that unlike the other hypertrophic signaling molecules tested here, cyclin D2 is an important regulator of both pathologic and physiological hypertrophy. Impact statement This research is relevant as the hypertrophic signaling pathways tested here have only been characterized for their role in pathological hypertrophy, and not in the context of exercise or physiological hypertrophy. By using the same transgenic mouse lines utilized in previous studies, our findings provide a novel and important understanding for the role of these signaling pathways in physiological hypertrophy. We found that alterations in the signaling pathways tested here had no impact on exercise performance. Exercise induced cardiac growth in all of the transgenic mice except for the mice deficient in cyclin D2. In the cyclin D2 null mice, cardiac function was not impacted even though the hypertrophic response was blunted and a number of signaling pathways are differentially regulated by exercise. These data provide the field with an understanding that cyclin D2 is a key mediator of physiological hypertrophy.

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