Skeletal muscle as potential central link between sarcopenia and immune senescence

Nelke, Christopher; Dziewas, Rainer; Minnerup, Jens; Meuth, Sven G.; Ruck, Tobias

doi:10.1016/j.ebiom.2019.10.034

Cited by 257 publications

(253 citation statements)

References 75 publications

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“…Skeletal muscle is recognized as an endocrine organ [260] which secretes cytokines (known as myokines) such as IL-6 [261], IL-7 [262], and IL-15 [263] in response to physical activity. Changes in circulating levels of these myokines, resulting from the various aspects of the aging process including increased inflammation and sarcopenia, are believed to play a role in the age-associated impairment of the immune response (immunosenescence) [264]. This highlights another mechanism by which sarcopenia may impact the health of older adults.…”

Section: Immune Function and Risk Of Covid-19 Infectionmentioning

confidence: 99%

Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss

et al. 2020

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The COVID-19 pandemic is an extraordinary global emergency that has led to the implementation of unprecedented measures in order to stem the spread of the infection. Internationally, governments are enforcing measures such as travel bans, quarantine, isolation, and social distancing leading to an extended period of time at home. This has resulted in reductions in physical activity and changes in dietary intakes that have the potential to accelerate sarcopenia, a deterioration of muscle mass and function (more likely in older populations), as well as increases in body fat. These changes in body composition are associated with a number of chronic, lifestyle diseases including cardiovascular disease (CVD), diabetes, osteoporosis, frailty, cognitive decline, and depression. Furthermore, CVD, diabetes, and elevated body fat are associated with greater risk of COVID-19 infection and more severe symptomology, underscoring the importance of avoiding the development of such morbidities. Here we review mechanisms of sarcopenia and their relation to the current data on the effects of COVID-19 confinement on physical activity, dietary habits, sleep, and stress as well as extended bed rest due to COVID-19 hospitalization. The potential of these factors to lead to an increased likelihood of muscle loss and chronic disease will be discussed. By offering a number of home-based strategies including resistance exercise, higher protein intakes and supplementation, we can potentially guide public health authorities to avoid a lifestyle disease and rehabilitation crisis post-COVID-19. Such strategies may also serve as useful preventative measures for reducing the likelihood of sarcopenia in general and in the event of future periods of isolation.

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Section: Immune Function and Risk Of Covid-19 Infectionmentioning

confidence: 99%

Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss

et al. 2020

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“…Therefore, in terms of biological aspect, low BMI may be primary connected with the susceptible background to infectious disease. Recent studies have revealed the skeletal muscle plays as a major immune regulatory organ by generating myokines which have anti-inflammatory and immunoprotective effects [18,19]. This pathological involvement in subjects with lower BMI needs to be calrified in future in terms of muscle volume of low BMI in CKD.…”

Section: Discussionmentioning

confidence: 99%

Impact of lower body mass index on risk of all-cause mortality and infection-related death in Japanese chronic kidney disease patients

et al. 2020

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Background: Several studies have reported that lower body mass index (BMI) is associated with high mortality in patients with chronic kidney disease (CKD). Rate of infection-related death in CKD patients is increasing. However, the relationship between BMI and infection-related death is unclear. Methods: Overall, 2648 CKD outpatients (estimated glomerular filtration rate < 60 mL/min and/or presenting with proteinuria) under the care of nephrologists were prospectively followed for 5 years. Patients were stratified by quartile of BMI levels. Data on all-cause mortality before progression to end-stage kidney disease (ESKD) and the cause of death were collected. Results: The median follow-up time was 3.9 years (interquartile range, 1.7-5.0); 114 patients died and 308 started renal replacement therapy. The leading causes of death were as follows; cardiovascular (41%), infection-related (21%), and malignancy-related (18%). Advanced age and lower BMI were the significant risk factors for all-cause mortality before progression to ESKD. Advanced age was statistically associated with respective causes of death, while lower BMI was associated with infection-related death only. CKD stage had no significant impact on all-cause or individual mortality. Conclusions: Low BMI was associated with significant risk of all-cause mortality and infection-related death, which may indicate the novel clinical target to improve CKD outcomes.

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“…IL-15 reduces adipose mass and also induces mitochondrial activity in adipose tissue [40][41][42][43], and IL-15 mRNA level and plasma concentration are decreased by defective AMPK signaling, which indicates that IL-15 may function through the AMPK signaling pathway. In aged muscle, it was demonstrated that aging could impair IL-15 signaling with aging-induced defective AMPK activation [44,45].…”

Section: Role Of Autophagy In the Induction Of Sarcopenic Obesitymentioning

confidence: 99%

Dysregulated Autophagy Mediates Sarcopenic Obesity and Its Complications via AMPK and PGC1α Signaling Pathways: Potential Involvement of Gut Dysbiosis as a Pathological Link

Ryu

Choi

Yang

et al. 2020

IJMS

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Sarcopenic obesity (SOB), which is closely related to being elderly as a feature of aging, is recently gaining attention because it is associated with many other age-related diseases that present as altered intercellular communication, dysregulated nutrient sensing, and mitochondrial dysfunction. Along with insulin resistance and inflammation as the core pathogenesis of SOB, autophagy has recently gained attention as a significant mechanism of muscle aging in SOB. Known as important cellular metabolic regulators, the AMP-activated protein kinase (AMPK) and the peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α) signaling pathways play an important role in autophagy, inflammation, and insulin resistance, as well as mutual communication between skeletal muscle, adipose tissue, and the liver. Furthermore, AMPK and PGC-1α signaling pathways are implicated in the gut microbiome–muscle axis. In this review, we describe the pathological link between SOB and its associated complications such as metabolic, cardiovascular, and liver disease, falls and fractures, osteoarthritis, pulmonary disease, and mental health via dysregulated autophagy controlled by AMPK and/or PGC-1α signaling pathways. Here, we propose potential treatments for SOB by modulating autophagy activity and gut dysbiosis based on plausible pathological links.

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Skeletal muscle as potential central link between sarcopenia and immune senescence

Cited by 257 publications

References 75 publications

Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss

Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss

Impact of lower body mass index on risk of all-cause mortality and infection-related death in Japanese chronic kidney disease patients

Dysregulated Autophagy Mediates Sarcopenic Obesity and Its Complications via AMPK and PGC1α Signaling Pathways: Potential Involvement of Gut Dysbiosis as a Pathological Link

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