High CO2 Levels Cause Skeletal Muscle Atrophy via AMP-activated Kinase (AMPK), FoxO3a Protein, and Muscle-specific Ring Finger Protein 1 (MuRF1)

Jaitovich, Ariel; Angulo, Martín; Lecuona, Emilia; Dada, Laura A.; Welch, Lynn C.; Cheng, Yuan; Gusarova, Galina A.; Ceco, Ermelinda; Liu, Chang; Shigemura, Masahiko; Barreiro, Esther; Patterson, Cam; Nader, Gustavo A.; Sznajder, Jacob I.

doi:10.1074/jbc.m114.625715

Cited by 104 publications

(144 citation statements)

References 59 publications

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“…This is interesting because AMPK has been shown to phosphorylate FoxO3 on non-Akt sites, thereby increasing its transcriptional activity (31). Downstream targets of AMPK-activated FoxO3 include MuRF1 and autophagyrelated genes that contribute to the pathophysiology of muscle wasting (38,90).…”

Section: Tgf-␤mentioning

confidence: 99%

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Bilodeau

Coyne

Wing

2016

American Journal of Physiology-Cell Physiology

136

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Bilodeau PA, Coyne ES, Wing SS. The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation. Am J Physiol Cell Physiol 311: C392-C403, 2016. First published August 10, 2016; doi:10.1152/ajpcell.00125.2016.-Muscle atrophy complicates many diseases as well as aging, and its presence predicts both decreased quality of life and survival. Much work has been conducted to define the molecular mechanisms involved in maintaining protein homeostasis in muscle. To date, the ubiquitin proteasome system (UPS) has been shown to play an important role in mediating muscle wasting. In this review, we have collated the enzymes in the UPS whose roles in muscle wasting have been confirmed through loss-of-function studies. We have integrated information on their mechanisms of action to create a model of how they work together to produce muscle atrophy. These enzymes are involved in promoting myofibrillar disassembly and degradation, activation of autophagy, inhibition of myogenesis as well as in modulating the signaling pathways that control these processes. Many anabolic and catabolic signaling pathways are involved in regulating these UPS genes, but none appear to coordinately regulate a large number of these genes. A number of catabolic signaling pathways appear to instead function by inhibition of the insulin/IGF-I/protein kinase B anabolic pathway. This pathway is a critical determinant of muscle mass, since it can suppress key ubiquitin ligases and autophagy, activate protein synthesis, and promote myogenesis through its downstream mediators such as forkhead box O, mammalian target of rapamycin, and GSK3␤, respectively. Although much progress has been made, a more complete inventory of the UPS genes involved in mediating muscle atrophy, their mechanisms of action, and their regulation will be useful for identifying novel therapeutic approaches to this important clinical problem.hormones; muscle atrophy SKELETAL MUSCLE SERVES TWO essential functions, a contractile function for locomotion/maintenance of posture and a metabolic function as the protein reservoir of the body. The myofibers that make up the muscle consist primarily of myofibrillar proteins. The ability of the body to maintain posture or to move arises from the precise organization of myofibrillar proteins into a contractile unit called the sarcomere. The sarcomere consists of thick filaments containing primarily myosin that can slide over thin filaments containing primarily actin. Both types of filaments contain additional regulatory proteins and are linked to the ␣-actinin-containing Z disk, the thin filaments directly so and the thick filaments via titin. Vimentin and desmin are intermediate filaments that serve to anchor sarcomeres properly at the Z disks. These myofibrillar proteins, as well as the sarcoplasmic proteins, also serve as the protein reservoir of the body. Upon fasting, once hepatic glycogen stores are depleted, muscle protein degradation must be activated to provide amino acids to the liver for gluconeogenesis. These amino a...

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Section: Tgf-␤mentioning

confidence: 99%

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Bilodeau

Coyne

Wing

2016

American Journal of Physiology-Cell Physiology

136

View full text Add to dashboard Cite

show abstract

“…FoxOs are under the control of neurotransmitters (Liang et al, 2006) and glucocorticoids (Qin et al, 2014). FoxOs also regulate signals for cellular atrophy (Jaitovich et al, 2015), cellular morphology (Aranha et al, 2009) and adult neurogenesis and all of these physiological or pathological conditions contribute to the development of depression (Borre et al, 2014;Mahar et al, 2014;Anacker et al, 2013). Although the role of FoxOs in the process of depression is only beginning to be unveiled, it is reasonable at this time to hypothesize that FoxO transcription factors will be found to be pivotal mediators in psychiatric disorders.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Forkhead box O transcription factors as possible mediators in the development of major depression

et al. 2015

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“…More than 10 years of "permissive hypercapnia" ventilatory strategy even led some authors to propose the concept of "therapeutic hypercapnia" (6). Nevertheless, more recent studies have tempered such an enthusiasm by demonstrating harmful effects of CO 2 on the lung on the one hand (14,15), and on the pulmonary circulation and the right ventricle on the other hand (16,17).…”

Section: The Impact Of Hypercapnia In Ardsmentioning

confidence: 99%

Hypercapnia during acute respiratory distress syndrome: the tree that hides the forest!

Repessé¹,

Vieillard‐Baron²

2017

J. Thorac. Dis.

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High CO2 Levels Cause Skeletal Muscle Atrophy via AMP-activated Kinase (AMPK), FoxO3a Protein, and Muscle-specific Ring Finger Protein 1 (MuRF1)

Cited by 104 publications

References 59 publications

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation

Forkhead box O transcription factors as possible mediators in the development of major depression

Hypercapnia during acute respiratory distress syndrome: the tree that hides the forest!

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