The Association of Systemic Interleukin 6 and Interleukin 10 Levels with Sarcopenia in Elderly Patients with Chronic Obstructive Pulmonary Disease

Lin, Baiyang; Bai, Li; Wang, Shenglong; Hong, Lin

doi:10.2147/ijgm.s321229

Cited by 16 publications

(13 citation statements)

References 41 publications

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“…Further, a combination of pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 can lead to extreme muscle loss. 49 50 51 52 Insufficient total protein due to the body’s inability to synthesize protein and inadequate protein intake is contributing factor for severe muscle strength decreases in sarcopenia. 53 Aging leads to decreases in motor nerve cells and satellite cells, reducing the response of movement and the recovery of damaged muscle fibers signals.…”

Section: Treatmentmentioning

confidence: 99%

A Review of Sarcopenia Pathophysiology, Diagnosis, Treatment and Future Direction

2022

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Sarcopenia is a progressive and generalized loss of skeletal muscle mass and function. The prevalence of sarcopenia was reported to be up to 29% in older persons in the community healthcare setting. Sarcopenia diagnosis is confirmed by the presence of low muscle mass plus low muscle strength or low physical performance. Sarcopenia management options include non-pharmacological and pharmacological approaches. Non-pharmacological approaches include resistance exercise and adequate nutrition. Of the two, resistance exercise is the standard non-pharmacological treatment approach for sarcopenia with significant positive evidence. Some dietary approaches such as adequate intake of protein, vitamin D, antioxidant nutrients, and long-chain polyunsaturated fatty acid have been shown to have positive effects against sarcopenia. Currently, no specific drugs have been approved by the Food and Drug Administration for the treatment of sarcopenia. However, several agents, including growth hormone, anabolic or androgenic steroids, selective androgenic receptor modulators, protein anabolic agents, appetite stimulants, myostatin inhibitors, activating II receptor drugs, β-receptor blockers, angiotensin-converting enzyme inhibitors, and troponin activators, are recommended and have been shown to have variable efficacy. Future research should focus on sarcopenia biological pathway and improved diagnostic approaches such as biomarkers for early detection, development of consistently pre-eminent treatment methods for severe sarcopenia patients, and establishing sensitive measures for predicting sarcopenia treatment response.

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Section: Treatmentmentioning

confidence: 99%

A Review of Sarcopenia Pathophysiology, Diagnosis, Treatment and Future Direction

2022

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“…Previous studies proposed that STAT3 pathway activation was associated with the development of muscle atrophy in various endogenous diseases including sepsis (Zanders et al, 2022), cancer (Bonetto et al, 2011;Silva et al, 2015;Rupert et al, 2021), chronic obstructive pulmonary disease (Lin et al, 2021), myocardial failure (Janssen et al, 2005), chronic kidney diseases (Zhang et al, 2013), and degenerative muscle disease (Wada et al, 2017;Liang et al, 2018). Therefore, our data might have significance in conditions beyond muscle wasting associated with thermal burn injury.…”

Section: Discussionmentioning

confidence: 51%

“…Among various proinflammatory cytokines, interleukin (IL)-6 is an especially important hallmark of severe burn injuries because plasma IL-6 concentrations were correlated with burn severity and increased mortality (Pileri et al, 2008;Lantos et al, 2010;Shelhamer et al, 2015). In addition to the burn injuries, increased levels of circulatory IL-6 are present in other medical conditions, including sepsis (Zanders et al, 2022), COVID-19 (Kang et al, 2020;Ali and Kunugi, 2021;Mittal et al, 2021;Seixas et al, 2022;Soares et al, 2022), diabetes mellitus (Perry et al, 2016), cancer (Rupert et al, 2021), chronic obstructive pulmonary disease (Lin et al, 2021), myocardial failure (Janssen et al, 2005), and end-stage kidney disease (Zhang et al, 2013). The severe involuntary loss of skeletal muscle, termed muscle wasting, is observed in all these conditions, suggesting a potential role for IL-6 in their development (Muñoz-Cánoves et al, 2013;Guadagnin et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

C188-9, a specific inhibitor of STAT3 signaling, prevents thermal burn-induced skeletal muscle wasting in mice

et al. 2022

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Burn injury is the leading cause of death and disability worldwide and places a tremendous economic burden on society. Systemic inflammatory responses induced by thermal burn injury can cause muscle wasting, a severe involuntary loss of skeletal muscle that adversely affects the survival and functional outcomes of these patients. Currently, no pharmacological interventions are available for the treatment of thermal burn-induced skeletal muscle wasting. Elevated levels of inflammatory cytokines, such as interleukin-6 (IL-6), are important hallmarks of severe burn injury. The levels of signal transducer and activator of transcription 3 (STAT3)—a downstream component of IL-6 inflammatory signaling—are elevated with muscle wasting in various pro-catabolic conditions, and STAT3 has been implicated in the regulation of skeletal muscle atrophy. Here, we tested the effects of the STAT3-specific signaling inhibitor C188-9 on thermal burn injury-induced skeletal muscle wasting in vivo and on C2C12 myotube atrophy in vitro after the administration of plasma from burn model mice. In mice, thermal burn injury severity dependently increased IL-6 in the plasma and tibialis anterior muscles and activated the STAT3 (increased ratio of phospho-STAT3/STAT3) and ubiquitin-proteasome proteolytic pathways (increased Atrogin-1/MAFbx and MuRF1). These effects resulted in skeletal muscle atrophy and reduced grip strength. In murine C2C12 myotubes, plasma from burn mice activated the same inflammatory and proteolytic pathways, leading to myotube atrophy. In mice with burn injury, the intraperitoneal injection of C188-9 (50 mg/kg) reduced activation of the STAT3 and ubiquitin-proteasome proteolytic pathways, reversed skeletal muscle atrophy, and increased grip strength. Similarly, pretreatment of murine C2C12 myotubes with C188-9 (10 µM) reduced activation of the same inflammatory and proteolytic pathways, and ameliorated myotube atrophy induced by plasma taken from burn model mice. Collectively, these results indicate that pharmacological inhibition of STAT3 signaling may be a novel therapeutic strategy for thermal burn-induced skeletal muscle wasting.

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“…These results indicate that the anti-inflammatory potential of IL-10 in elderly individuals with sarcopenia is not sufficient to overcome the basal pro-inflammatory status [ 102 ]. Nonetheless, elderly patients with Chronic Obstructive Pulmonary Disease diagnosed with sarcopenia presented high levels of IL-6 but not IL-10 [ 103 ].…”

Section: Cytokines/myokines ( Friends or Foes )mentioning

confidence: 99%

Inflammaging: Implications in Sarcopenia

Antuña

Cachán-Vega

Bermejo-Millo

et al. 2022

IJMS

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In a world in which life expectancy is increasing, understanding and promoting healthy aging becomes a contemporary demand. In the elderly, a sterile, chronic and low-grade systemic inflammation known as “inflammaging” is linked with many age-associated diseases. Considering sarcopenia as a loss of strength and mass of skeletal muscle related to aging, correlations between these two terms have been proposed. Better knowledge of the immune system players in skeletal muscle would help to elucidate their implications in sarcopenia. Characterizing the activators of damage sensors and the downstream effectors explains the inference with skeletal muscle performance. Sarcopenia has also been linked to chronic diseases such as diabetes, metabolic syndrome and obesity. Implications of inflammatory signals from these diseases negatively affect skeletal muscle. Autophagic mechanisms are closely related with the inflammasome, as autophagy eliminates stress signaling sent by damage organelles, but also acts with an immunomodulatory function affecting immune cells and cytokine release. The use of melatonin, an antioxidant, ROS scavenger and immune and autophagy modulator, or senotherapeutic compounds targeting senescent cells could represent strategies to counteract inflammation. This review aims to present the many factors regulating skeletal muscle inflammaging and their major implications in order to understand the molecular mechanisms involved in sarcopenia.

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The Association of Systemic Interleukin 6 and Interleukin 10 Levels with Sarcopenia in Elderly Patients with Chronic Obstructive Pulmonary Disease

Cited by 16 publications

References 41 publications

A Review of Sarcopenia Pathophysiology, Diagnosis, Treatment and Future Direction

A Review of Sarcopenia Pathophysiology, Diagnosis, Treatment and Future Direction

C188-9, a specific inhibitor of STAT3 signaling, prevents thermal burn-induced skeletal muscle wasting in mice

Inflammaging: Implications in Sarcopenia

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