Is inflammatory signaling involved in disease-related muscle wasting? Evidence from osteoarthritis, chronic obstructive pulmonary disease and type II diabetes

Dalle, Sebastiaan; Koppo, Katrien

doi:10.1016/j.exger.2020.110964

Cited by 50 publications

(47 citation statements)

References 193 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This indicates that the reduced force generating capacity might also be related to alterations in the dystrophin glycoprotein complex (Acharyya et al 2005), mitochondrial dysfunctions (Antunes et al 2014) and/or a reduction in the strongly bound cross-bridges (Toth et al 2013). At a molecular level, it was suggested that functional deficits in cachexia are related to muscle inflammatory signaling (Dalle et al 2017;VanderVeen et al 2018;Dalle and Koppo 2020). Interestingly, the SOL was resistant to cachexiainduced muscle functional impairments.…”

Section: Discussionmentioning

confidence: 99%

Voluntary exercise does not improve muscular properties or functional capacity during C26-induced cancer cachexia in mice

Hiroux

Dalle

Koppo

et al. 2021

J Muscle Res Cell Motil

Self Cite

View full text Add to dashboard Cite

Exercise training is considered as a potential intervention to counteract muscle degeneration in cancer cachexia. However, evidence to support such intervention is equivocal. Therefore, we investigated the effect of exercise training, i.e. voluntary wheel running, on muscle wasting, functional capacity, fiber type composition and vascularization during experimental cancer cachexia in mice. Balb/c mice were injected with PBS (CON) or C26 colon carcinoma cells to induce cancer cachexia (C26). Mice had free access to a running wheel in their home cage (CONEX and C26EX, n=8-9) or were sedentary (CONS and C26S, n=8-9). Mice were sacrificed 18 days upon tumor cell injection. Immunohistochemical analyes were performed on m. gastrocnemius and quadriceps, and ex vivo contractile properties were assessed in m. soleus and extensor digitorum longus (EDL). Compared with CON, C26 mice exhibited body weight loss (~20%), muscle atrophy (~25%), reduced grip strength (~25%), and lower twitch and tetanic force (~20%) production in EDL but not in m. soleus. Furthermore, muscle of C26 mice were characterizd by a slow-to-fast fiber type shift (type IIx fibers: +57%) and increased capillary density (~30%). In C26 mice, wheel running affect neither body weight loss, nor muscle atrophy or functional capacity, nor inhibited tumor growth. However, wheel running induced a type IIb to type IIa fiber shift in m. quadriceps from both CON and C26, but not in m. gastrocnemius. Wheel running does not exacerbate muscular degeneration in cachexic mice, but, when voluntary, is insufficient to improve the muscle phenotype.

show abstract

Section: Discussionmentioning

confidence: 99%

Voluntary exercise does not improve muscular properties or functional capacity during C26-induced cancer cachexia in mice

Hiroux

Dalle

Koppo

et al. 2021

J Muscle Res Cell Motil

Self Cite

View full text Add to dashboard Cite

show abstract

“…Multiple factors contribute to age-related muscle wasting, e.g. inflammation 8 , 9 , malnutrition 10 , metabolic dysregulations 11 and physical inactivity 12 . Recently, there is a growing interest in the role of the cannabinoid system in controlling plasticity in metabolic tissues, such as adipose tissue and skeletal muscle 13 – 15 .…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid receptor 1 expression is higher in muscle of old vs. young males, and increases upon resistance exercise in older adults

Dalle

Koppo

2021

Sci Rep

Self Cite

View full text Add to dashboard Cite

Aged skeletal muscle undergoes metabolic and structural alterations eventually resulting in a loss of muscle strength and mass, i.e. age-related sarcopenia. Therefore, novel targets for muscle growth purposes in elderly are needed. Here, we explored the role of the cannabinoid system in muscle plasticity through the expression of muscle cannabinoid receptors (CBs) in young and old humans. The CB1 expression was higher (+ 25%; p = 0.04) in muscle of old (≥ 65 years) vs. young adults (20–27 years), whereas CB2 was not differently expressed. Furthermore, resistance exercise tended to increase the CB1 (+ 11%; p = 0.055) and CB2 (+ 37%; p = 0.066) expression in muscle of older adults. Interestingly, increases in the expression of CB2 following resistance exercise positively correlated with changes in key mechanisms of muscle homeostasis, such as catabolism (FOXO3a) and regenerative capacity (Pax7, MyoD). This study for the first time shows that CB1 is differentially expressed with aging and that changes in CB2 expression upon resistance exercise training correlate with changes in mediators that play a central role in muscle plasticity. These data confirm earlier work in cells and mice showing that the cannabinoid system might orchestrate muscle growth, which is an incentive to further explore CB-based strategies that might counteract sarcopenia.

show abstract

“…Kwang Byun et al [ 46 ] correlated systemic inflammation present in chronic obstructive pulmonary disease (COPD) with sarcopenia. Similarly, Dalle et al [ 47 ] demonstrated that three apparently different pathological states (i.e., type II diabetes, osteoarthritis, and COPD) are associated with an inflammatory state and lead to sarcopenia. Interestingly, a latent inflammatory state such as IBD also correlates to a greater onset of sarcopenia [ 14 , 48 ].…”

Section: The Importance Of Micrornasmentioning

confidence: 98%

Sarcopenia: Etiology, Nutritional Approaches, and miRNAs

Cannataro

Carbone

Petro

et al. 2021

IJMS

101

View full text Add to dashboard Cite

Sarcopenia, an age-related decline in skeletal muscle mass and function, dramatically affects the quality of life. Although there is a consensus that sarcopenia is a multifactorial syndrome, the etiology and underlying mechanisms are not yet delineated. Moreover, research about nutritional interventions to prevent the development of sarcopenia is mainly focused on the amount and quality of protein intake. The impact of several nutrition strategies that consider timing of food intake, anti-inflammatory nutrients, metabolic control, and the role of mitochondrial function on the progression of sarcopenia is not fully understood. This narrative review summarizes the metabolic background of this phenomenon and proposes an integral nutritional approach (including dietary supplements such as creatine monohydrate) to target potential molecular pathways that may affect reduce or ameliorate the adverse effects of sarcopenia. Lastly, miRNAs, in particular those produced by skeletal muscle (MyomiR), might represent a valid tool to evaluate sarcopenia progression as a potential rapid and early biomarker for diagnosis and characterization.

show abstract

Is inflammatory signaling involved in disease-related muscle wasting? Evidence from osteoarthritis, chronic obstructive pulmonary disease and type II diabetes

Cited by 50 publications

References 193 publications

Voluntary exercise does not improve muscular properties or functional capacity during C26-induced cancer cachexia in mice

Voluntary exercise does not improve muscular properties or functional capacity during C26-induced cancer cachexia in mice

Cannabinoid receptor 1 expression is higher in muscle of old vs. young males, and increases upon resistance exercise in older adults

Sarcopenia: Etiology, Nutritional Approaches, and miRNAs

Contact Info

Product

Resources

About