The role of myokines in muscle health and disease

Lightfoot, Adam P.; Cooper, Robert G.

doi:10.1097/bor.0000000000000337

Cited by 65 publications

(52 citation statements)

References 47 publications

(48 reference statements)

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“…Interleukin‐6 has an established role in exercise‐ and disease‐induced changes to systemic and skeletal muscle metabolism (Febbraio & Pedersen, ; Febbraio et al., ; Lightfoot & Cooper, ; Wolf, Rose‐John, & Garbers, ). Although elevating the circulating IL‐6 for 2 weeks through overexpression of an IL‐6 plasmid has been shown to accelerate cachexia in tumour‐bearing mice and disrupt muscle metabolism in tumour‐free mice (Carson & Baltgalvis, ; Puppa et al., ; White et al., ), whether IL‐6 disrupts skeletal muscle mitochondrial function and muscle fatigability has not been measured.…”

Section: Discussionmentioning

confidence: 99%

“…Although chronic inflammation is a non‐specific immune response, cytokines are inflammatory mediators that have been implicated in the progression of several diseases and associated co‐morbidities (Deans & Wigmore, ; Fearon, Glass, & Guttridge, ; Lightfoot & Cooper, ; Zhou, Liu, Liang, Li, & Song, ). In addition to tumour growth and development, elevated circulating IL‐6 has been linked to disrupted protein turnover associated with cancer‐induced muscle wasting (Carson & Baltgalvis, ; Cron, Allen, & Febbraio, ; Narsale & Carson, ).…”

Section: Discussionmentioning

confidence: 99%

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The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin‐6

VanderVeen

Fix

Montalvo

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Interleukin‐6 has been associated with muscle mass and metabolism in both physiological and pathological conditions. A causal role for interleukin‐6 in the induction of fatigue and disruption of mitochondrial function has not been determined. What is the main finding and its importance?We demonstrate that chronically elevated interleukin‐6 increased skeletal muscle fatigability and disrupted mitochondrial content and function independent of changes in fibre type and mass. Abstract Interleukin‐6 (IL‐6) can initiate intracellular signalling in skeletal muscle by binding to the IL‐6‐receptor and interacting with the transmembrane gp130 protein. Circulating IL‐6 has established effects on skeletal muscle mass and metabolism in both physiological and pathological conditions. However, the effects of circulating IL‐6 on skeletal muscle function are not well understood. The purpose of this study was to determine whether chronically elevated systemic IL‐6 was sufficient to disrupt skeletal muscle force, fatigue and mitochondrial function. Additionally, we examined the role of muscle gp130 signalling during overexpression of IL‐6. Systemic IL‐6 overexpression for 2 weeks was achieved by electroporation of an IL‐6 overexpression plasmid or empty vector into the quadriceps of either C57BL/6 (WT) or skeletal muscle gp130 knockout (KO) male mice. Tibialis anterior muscle in situ functional properties and mitochondrial respiration were determined. Interleukin‐6 accelerated in situ skeletal muscle fatigue in the WT, with a 18.5% reduction in force within 90 s of repeated submaximal contractions and a 7% reduction in maximal tetanic force after 5 min. There was no difference between fatigue in the KO and KO+IL‐6. Interleukin‐6 reduced WT muscle mitochondrial respiratory control ratio by 36% and cytochrome c oxidase activity by 42%. Interleukin‐6 had no effect on either KO respiratory control ratio or cytochrome c oxidase activity. Interleukin‐6 also had no effect on body weight, muscle mass or tetanic force in either genotype. These results provide evidence that 2 weeks of elevated systemic IL‐6 is sufficient to increase skeletal muscle fatigability and decrease muscle mitochondrial content and function, and these effects require muscle gp130 signalling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin‐6

VanderVeen

Fix

Montalvo

et al. 2019

Experimental Physiology

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“…[16][17][18] The rising prevalence of insulin resistance in the general population highlights the need for a better understanding of its pathogenesis. 2,3,21,[25][26][27] One of the most intriguing biological activities of myokines is their ability to modulate insulin action and metabolism of specific cells which is almost certainly of significant biomedical importance. [19][20][21][22] While the muscle responds directly to insulin by translocation of GLUT4 to the sarcoplasmic membrane, myokines likewise influence whole-body metabolism of glucose and lipids, as they have been repeatedly shown to act on adipose, liver, pancreas and intestine tissues.…”

Section: Introductionmentioning

confidence: 99%

Myokines in skeletal muscle physiology and metabolism: Recent advances and future perspectives

2019

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Myokines are molecules produced and secreted by skeletal muscle to act in an auto-, para-and endocrine manner to alter physiological function of target tissues. The growing number of effects of myokines on metabolism of distant tissues provides a compelling case for crosstalk between skeletal muscle and other tissues and organs to regulate metabolic homoeostasis. In this review, we summarize and discuss the current knowledge regarding the impact on metabolism of several canonical and recently identified myokines. We focus specifically on myostatin, β-aminoisobutyric acid, interleukin-15, meteorin-like and myonectin, and discuss how these myokines are induced and regulated as well as their overall function. We also review how these myokines may serve as potential prognostic biomarkers that reflect whole-body metabolism and how they may be attractive therapeutic targets for treating muscle and metabolic diseases. K E Y W O R D Sinterleukin-15, metabolism, meteorin-like, myonectin, myostatin, β-aminoisobutyric acid

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“…Skeletal muscle is one of the major producers of interleukin-6 (IL-6), which contributes with other factors such as irisin to the fine regulation of bone metabolism and adipose tissue homeostasis after physical exercise [10, 97, 98]. The relationship between IL-6 and stroke is established principally by neuroinflammatory mechanisms in the CNS, where the expression of genes such as IL-6, besides myeloperoxidase (MPO), IL-1 β , and TNF- α , is fundamental for stroke susceptibility [99] but also myocardial stroke generates a peripheral proinflammatory response in skeletal muscle [100].…”

Section: Bone-skeletal Muscle Biomarkers In Strokementioning

confidence: 99%

“…Neuroinflammation represents the main mechanism underlying the onset and development of stroke and the peripheral level of soluble immune factors and immune cells should give insights either on the onset and pathogenesis of stroke or on its recovery [6–8]. Poststroke rehabilitation, particularly following physical exercise and training, generates a crowded mass of mediators, more than 90, called myokines, which plays an emerging role in the biomarker field, which should update the role of plasma or circulating markers in stroke [9, 10] (see Figure 1). …”

Section: Introductionmentioning

confidence: 99%

Assessed and Emerging Biomarkers in Stroke and Training-Mediated Stroke Recovery: State of the Art

et al. 2017

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Since the increasing update of the biomolecular scientific literature, biomarkers in stroke have reached an outstanding and remarkable revision in the very recent years. Besides the diagnostic and prognostic role of some inflammatory markers, many further molecules and biological factors have been added to the list, including tissue derived cytokines, growth factor-like molecules, hormones, and microRNAs. The literatures on brain derived growth factor and other neuroimmune mediators, bone-skeletal muscle biomarkers, cellular and immunity biomarkers, and the role of microRNAs in stroke recovery were reviewed. To date, biomarkers represent a possible challenge in the diagnostic and prognostic evaluation of stroke onset, pathogenesis, and recovery. Many molecules are still under investigation and may become promising and encouraging biomarkers. Experimental and clinical research should increase this list and promote new discoveries in this field, to improve stroke diagnosis and treatment.

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The role of myokines in muscle health and disease

Abstract: Myokines appear to exert diverse beneficial effects, though their mechanistic roles in myositis and other myopathologies remain poorly understood.

Cited by 65 publications

References 47 publications

The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin‐6

The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin‐6

Myokines in skeletal muscle physiology and metabolism: Recent advances and future perspectives

Assessed and Emerging Biomarkers in Stroke and Training-Mediated Stroke Recovery: State of the Art

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