The IGF1-PI3K-Akt Signaling Pathway in Mediating Exercise-Induced Cardiac Hypertrophy and Protection

Weeks, Kate L.; Bernardo, Bianca C.; Ooi, Jenny Y. Y.; Patterson, Natalie L.; McMullen, Julie R.

doi:10.1007/978-981-10-4304-8_12

Cited by 78 publications

(61 citation statements)

References 154 publications

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“…Previous studies have shown that physiological cardiac hypertrophy is associated with an exerciseinduced increase in the levels of IGF-1 (Neri Serneri et al, 2001). We found that the cardiomyocyte surface area in response to IGF-1 for 48 hours was significantly larger than that of the non-stimulated H9C2 cells, and the levels of hypertrophy markers (ANP and BNP) were also significantly increased in mRNA levels, while leaving aactin mRNA unchanged, which is considered as a trigger for physiological cardiac hypertrophy (McMullen and Izumo, 2006;Weeks et al, 2017). Autophagy is a highly conserved and ubiquitous metabolic pathway in living organisms (Sandoval et al, 2008).…”

Section: Discussionmentioning

confidence: 69%

Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats

Luo

et al. 2020

Front. Genet.

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Exercise-induced autophagy is associated with physiological left ventricular hypertrophy (LVH), and a growing body of evidence suggests that microRNAs (miRNAs) can regulate autophagy-related genes. However, the precise role of miRNAs in exercise induced autophagy in physiological LVH has not been fully defined. In this study, we investigated the microRNA-autophagy axis in physiological LVH and deciphered the underlying mechanism using a rat swimming exercise model. Rats were assigned to sedentary control (CON) and swimming exercise (EX) groups; those in the latter group completed a 10-week swimming exercise without any load. For in vitro studies, H9C2 cardiomyocyte cell line was stimulated with IGF-1 for hypertrophy. We found a significant increase in autophagy activity in the hearts of rats with exercise-induced physiological hypertrophy, and miRNAs showed a high score in the pathway enriched in autophagy. Moreover, the expression levels of miR-26b-5p, miR-204-5p, and miR-497-3p showed an obvious increase in rat hearts. Adenovirus-mediated overexpression of miR-26b-5p, miR-204-5p, and miR-497-3p markedly attenuated IGF-1-induced hypertrophy in H9C2 cells by suppressing autophagy. Furthermore, attenuated autophagy in H9C2 cells through targeting ULK1, LC3B, and Beclin 1, respectively. Taken together, our results demonstrate that swimming exercise induced physiological LVH, at least in part, by modulating the microRNA-autophagy axis, and that miR-26b-5p, miR-204-5p, and miR-497-3p may help distinguish physiological and pathological LVH.

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Section: Discussionmentioning

confidence: 69%

Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats

Luo

et al. 2020

Front. Genet.

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“…The results of our study help to generate hypotheses to be tested in future studies. It is known that signaling pathways and molecular mechanisms responsible for mediating pathological versus physiological cardiac hypertrophy induced by long‐term exercise training are different (Weeks, Bernardo, Ooi, Patterson, & McMullen, ). The insulin‐like growth factor 1 ( IGF1 ) signaling pathway regulates exercise‐induced physiological cardiac hypertrophy and cardiac protection (Weeks et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…It is known that signaling pathways and molecular mechanisms responsible for mediating pathological versus physiological cardiac hypertrophy induced by long‐term exercise training are different (Weeks, Bernardo, Ooi, Patterson, & McMullen, ). The insulin‐like growth factor 1 ( IGF1 ) signaling pathway regulates exercise‐induced physiological cardiac hypertrophy and cardiac protection (Weeks et al, ). Tereshchenko et al recently identified a GEH‐associated genetic polymorphism in the intron of the IGF1 ‐receptor ( IGF1R ) gene (Tereshchenko et al, ).…”

Section: Discussionmentioning

confidence: 99%

Vectorcardiogram in athletes: The Sun Valley Ski Study

Thomas

Alday

Junell

et al. 2018

Noninvasive Electrocardiol

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Background Global electrical heterogeneity (GEH) is associated with sudden cardiac death (SCD) in adults of 45 years and above. However, GEH has not been previously measured in young athletes. The goal of this study was to establish a reference for vectorcardiograpic (VCG) metrics in male and female athletes. Methods Skiers (n = 140; mean age 19.2 ± 3.5 years; 66% male, 94% white; 53% professional athletes) were enrolled in a prospective cohort. Resting 12‐lead ECGs were interpreted per the International ECG criteria. Associations of age, sex, and athletic performance with GEH were studied. Results In age and training level‐adjusted analyses, male sex was associated with a larger T vector [T peak magnitude +186 (95% CI 106–266) µV] and a wider spatial QRS‐T angle [+28.2 (17.3–39.2)°] as compared to women. Spatial QRS‐T angle in the ECG left ventricular hypertrophy (LVH) voltage group (n = 21; 15%) and normal ECG group did not differ (67.7 ± 25.0 vs. 66.8 ± 28.2; p = 0.914), suggesting that ECG LVH voltage in athletes reflects physiological remodeling. In contrast, skiers with right ventricular hypertrophy (RVH) voltage (n = 26, 18.6%) had wider QRS‐T angle (92.7 ± 29.6 vs. 66.8 ± 28.2°; p = 0.001), larger SAI QRST (194.9 ± 30.2 vs. 157.8 ± 42.6 mV × ms; p < 0.0001), but similar peak SVG vector magnitude (1976 ± 548 vs. 1939 ± 395 µV; p = 0.775) as compared to the normal ECG group. Better athletic performance was associated with the narrower QRS‐T angle. Each 10% worsening in an athlete's Federation Internationale de’ Ski downhill ranking percentile was associated with an increase in spatial QRS‐T angle by 2.1 (95% CI 0.3–3.9) degrees (p = 0.013). Conclusion Vectorcardiograpic adds nuances to ECG phenomena in athletes.

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“…IGF1 is associated with the process of cardiac hypertrophy closely and substantial essays have indicated that it is an active regulator in cardiac hypertrophy. IGF1‐PI3K‐Akt signaling pathway has been manifested to regulate cardiac hypertrophy (Weeks et al, 2017). In this study, we found that IGF1 served as a downstream target of miR‐182‐5p.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR‐182‐5p/IGF1 axis

Wang

Lin

Zhang

2020

Cell Biology International

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Long non‐coding RNA (lncRNA) SNHG16 has been reported to be significant regulators in multiple cancers. However, never has the relationship between it and cardiac hypertrophy been studied until now. In this study, angiotensin II (Ang II)‐treated cardiomyocytes isolated from neonatal mice were used as a model of cardiac hypertrophy in vitro. Real‐time quantitative polymerase chain reaction was performed to measure the expression of SNHG16, miR‐182‐5p, and insulin‐like growth factor 1 (IGF1). The relationship between SNHG16 and its downstream genes were corroborated by RNA pull‐down and luciferase reporter experiments. Western blot was conducted to detect the expression of markers of hypertrophy. The results disclosed that SNHG16 expression was in a high level in the cardiac hypertrophic model. Down‐regulation of SNHG16 could decline the expression of hypertrophic markers and reduce cell surface area induced by Ang II. Moreover, SNHG16 was discovered to be activated by transcription factor CCCTC‐binding factor. In addition, SNHG16 could enlarge cell surface area and increase the expression of hypertrophic markers by inhibiting miR‐182‐5p expression in Ang II‐treated cardiomyocytes. Finally, overexpression of IGF1 could rescue the effects of silenced SNHG16 on cardiac hypertrophy cells. In brief, our study illustrated that silenced SNHG16 repressed Ang II‐imposed cardiac hypertrophy via targeting miR‐182‐5p/IGF1 axis.

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The IGF1-PI3K-Akt Signaling Pathway in Mediating Exercise-Induced Cardiac Hypertrophy and Protection

Cited by 78 publications

References 154 publications

Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats

Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p Expression Facilitates Exercise-Induced Physiological Cardiac Hypertrophy by Augmenting Autophagy in Rats

Vectorcardiogram in athletes: The Sun Valley Ski Study

Up‐regulation of SNHG16 induced by CTCF accelerates cardiac hypertrophy by targeting miR‐182‐5p/IGF1 axis

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