Potential role of lipin-1 in exercise-induced mitochondrial biogenesis

2008 ◽  
Vol 374 (3) ◽  
pp. 587-591 ◽  
Author(s):  
Kazuhiko Higashida ◽  
Mitsuru Higuchi ◽  
Shin Terada
Keyword(s):  
Mitochondrial Biogenesis ◽  
Potential Role ◽  
Lipin 1 ◽  
Exercise Induced

scholarly journals PGC-1α regulation by exercise training and its influences on muscle function and insulin sensitivity

2010 ◽  
Vol 299 (2) ◽  
pp. E145-E161 ◽  
Author(s):  
Vitor A. Lira ◽  
Carley R. Benton ◽  
Zhen Yan ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Transgenic Mice ◽  
Mitochondrial Biogenesis ◽  
Therapeutic Potential ◽  
Fiber Type ◽  
Acid Oxidation ◽  
Physiological Limits ◽  
Exercise Induced

The peroxisome proliferator-activated receptor-γ (PPARγ) coactivator-1α (PGC-1α) is a major regulator of exercise-induced phenotypic adaptation and substrate utilization. We provide an overview of 1) the role of PGC-1α in exercise-mediated muscle adaptation and 2) the possible insulin-sensitizing role of PGC-1α. To these ends, the following questions are addressed. 1) How is PGC-1α regulated, 2) what adaptations are indeed dependent on PGC-1α action, 3) is PGC-1α altered in insulin resistance, and 4) are PGC-1α-knockout and -transgenic mice suitable models for examining therapeutic potential of this coactivator? In skeletal muscle, an orchestrated signaling network, including Ca2+-dependent pathways, reactive oxygen species (ROS), nitric oxide (NO), AMP-dependent protein kinase (AMPK), and p38 MAPK, is involved in the control of contractile protein expression, angiogenesis, mitochondrial biogenesis, and other adaptations. However, the p38γ MAPK/PGC-1α regulatory axis has been confirmed to be required for exercise-induced angiogenesis and mitochondrial biogenesis but not for fiber type transformation. With respect to a potential insulin-sensitizing role of PGC-1α, human studies on type 2 diabetes suggest that PGC-1α and its target genes are only modestly downregulated (≤34%). However, studies in PGC-1α-knockout or PGC-1α-transgenic mice have provided unexpected anomalies, which appear to suggest that PGC-1α does not have an insulin-sensitizing role. In contrast, a modest (∼25%) upregulation of PGC-1α, within physiological limits, does improve mitochondrial biogenesis, fatty acid oxidation, and insulin sensitivity in healthy and insulin-resistant skeletal muscle. Taken altogether, there is substantial evidence that the p38γ MAPK-PGC-1α regulatory axis is critical for exercise-induced metabolic adaptations in skeletal muscle, and strategies that upregulate PGC-1α, within physiological limits, have revealed its insulin-sensitizing effects.

The Potential Role of Exercise-Induced Muscle Damage in Exertional Heat Stroke

2021 ◽  
Vol 51 (5) ◽  
pp. 863-872
Author(s):  
Zidong Li ◽  
Zachary J. McKenna ◽  
Matthew R. Kuennen ◽  
Flávio de Castro Magalhães ◽  
Christine M. Mermier ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Potential Role ◽  
Heat Stroke ◽  
Exertional Heat Stroke ◽  
Exercise Induced

scholarly journals Potential Role of Structural Variants of Circulating Lipopolysaccharide in Exercise‐Induced Heat Illness

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Skylar Wright ◽  
Yuri Hosokawa ◽  
Ekow C Dadzie ◽  
Virgilio Lopez ◽  
Abigail T Colburn ◽  
...  
Keyword(s):  
Potential Role ◽  
Heat Illness ◽  
Structural Variants ◽  
Exercise Induced

P5399microRNA-486 mediates exercise-induced cardiac growth and prevents cardiac ischemia-reperfusion injury

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Bei ◽  
D Lu ◽  
X Meng ◽  
Y Zhu ◽  
X Liang ◽  
...  
Keyword(s):  
Infarct Size ◽  
Potential Role ◽  
Target Genes ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Heart Weight ◽  
Cardiac Growth ◽  
Intramyocardial Injection ◽  
Exercise Induced

Abstract Background Molecules mediating exercise-induced physiological cardiac growth may be beneficial to prevent cardiac injury and remodeling. MicroRNA-486 (miR-486) is a muscle-enriched microRNA which was found to be increased in exercised heart. However, the role of miR-486 in exercise-induced cardiac growth is largely unknown. Purpose We aimed to study the function of miR-486 in exercise-induced cardiac growth, and to investigate its potential role in protection against cardiac ischemia/reperfusion (I/R) injury. Methods Male C57BL/6 adult mice were subjected to 3-week swimming exercise to induce physiological cardiac growth. Knockdown of miR-486 was performed by intramyocardial injection of miR-486 sponge to evaluate the role of miR-486 in exercise-induced cardiac growth. Moreover, intramyocardial injection of miR-486 overexpression lentivirus was performed to investigate whether miR-486 could reduce infarct size in mice suffered from acute I/R injury (30 min ligation and 24 hr reperfusion of left anterior descending coronary artery). Meanwhile, the functional role of miR-486 was evaluated in neonatal rat cardiomyocytes (NRCMs) treated with oxygen glucose deprivation/reperfusion (OGDR) using Tunel staining. Finally, function-rescue assays were performed to identify target genes of miR-486. Results Exercise significantly upregulated miR-486 in the heart, which was reduced by intramyocardial injection of miR-486 sponge. Exercise induced-cardiac growth was abolished in mice with intramyocardial injection of miR-486 sponge, as evidenced by reduced heart weight/body weight ratio and heart weight/tibia length ratio compared to control exercised-mice, suggesting a potential role of miR-486 in mediating exercise-induced cardiac growth. Meanwhile, we found that intramyocardial injection of miR-486 overexpression lentivirus was able to reduce the infarct size as determined by TTC staining. Moreover, in OGDR-induced apoptosis of NRCMs, miR-486 mimics was able to reduce cardiomyocyte apoptosis, while miR-486 inhibitor performed the opposite. Finally, PTEN and FoxO1 were identified as target genes of miR-486 in the control of cardiomyocyte apoptosis. Conclusions miR-486 mediates exercise-induced cardiac growth and protects against cardiac I/R injury. Increasing miR-486 might serve as a potential target to reduce myocardial apoptosis upon I/R injury. Acknowledgement/Funding This work was supported by the grants from National Natural Science Foundation of China 81722008, 91639101 and 81570362 to JJ Xiao, 81770401 to Y Bei

scholarly journals Exercise intolerance and fatigue in chronic heart failure: is there a role for group III/IV afferent feedback?

2020 ◽  
Vol 27 (17) ◽  
pp. 1862-1872
Author(s):  
Luca Angius ◽  
Antonio Crisafulli
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Potential Role ◽  
Muscle Afferents ◽  
Afferent Feedback ◽  
Exercise Intolerance ◽  
Peripheral Fatigue ◽  
Group Iii ◽  
Exercise Induced

Exercise intolerance and early fatiguability are hallmark symptoms of chronic heart failure. While the malfunction of the heart is certainly the leading cause of chronic heart failure, the patho-physiological mechanisms of exercise intolerance in these patients are more complex, multifactorial and only partially understood. Some evidence points towards a potential role of an exaggerated afferent feedback from group III/IV muscle afferents in the genesis of these symptoms. Overactivity of feedback from these muscle afferents may cause exercise intolerance with a double action: by inducing cardiovascular dysregulation, by reducing motor output and by facilitating the development of central and peripheral fatigue during exercise. Importantly, physical inactivity appears to affect the progression of the syndrome negatively, while physical training can partially counteract this condition. In the present review, the role played by group III/IV afferent feedback in cardiovascular regulation during exercise and exercise-induced muscle fatigue of healthy people and their potential role in inducing exercise intolerance in chronic heart failure patients will be summarised.

scholarly journals Potential role of exercise-induced glucose-6-phosphate isomerase in skeletal muscle function

2019 ◽  
Vol 23 (2) ◽  
pp. 28-33 ◽  
Author(s):  
Seong Eun Kwak ◽  
Hyung Eun Shin ◽  
Di Di Zhang ◽  
Jihyun Lee ◽  
Kyung Jin Yoon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Potential Role ◽  
Skeletal Muscle Function ◽  
Exercise Induced

POPDC proteins and cardiac function

2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand
Keyword(s):  
Potential Role ◽  
Striated Muscle ◽  
Short Review ◽  
Effector Proteins ◽  
Muscle Disease ◽  
Disease Genes ◽  
Protein Protein Interaction ◽  
Interaction Partners ◽  
And Function

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.

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