Nuclear factor-kappa B signaling in skeletal muscle atrophy

Li, Hong; Malhotra, Shweta; Kumar, Ashok

doi:10.1007/s00109-008-0373-8

Cited by 372 publications

(508 citation statements)

References 101 publications

(201 reference statements)

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“…NF-kB activation in the skeletal muscle of COPD patients may be sufficient for the induction of muscle atrophy [82,83]. Conversely, inhibition of NF-kB restores muscle mass in a number of experimental models of atrophy, implying an important role for NF-kB in this process.…”

Section: Mechanismsmentioning

confidence: 99%

“…NF-kB activation is also implicated in mediating systemic inflammation and may be involved in skeletal muscle weakness in COPD patients [82]. NF-kB activation is important in skeletal muscle atrophy and the inhibition of NF-kB may prevent this in animals [83]. NF-kB activation has also been implicated in several of the comorbidities associated with COPD, including cardiovascular disease, lung cancer, osteoporosis and diabetes [208].…”

Section: Pde4 Inhibitorsmentioning

confidence: 99%

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Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

European Respiratory Journal

1,465

1,113

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Increasing evidence indicates that chronic obstructive pulmonary disease (COPD) is a complex disease involving more than airflow obstruction. Airflow obstruction has profound effects on cardiac function and gas exchange with systemic consequences. In addition, as COPD results from inflammation and/or alterations in repair mechanisms, the ''spill-over'' of inflammatory mediators into the circulation may result in important systemic manifestations of the disease, such as skeletal muscle wasting and cachexia. Systemic inflammation may also initiate or worsen comorbid diseases, such as ischaemic heart disease, heart failure, osteoporosis, normocytic anaemia, lung cancer, depression and diabetes. Comorbid diseases potentiate the morbidity of COPD, leading to increased hospitalisations, mortality and healthcare costs. Comorbidities complicate the management of COPD and need to be evaluated carefully. Current therapies for comorbid diseases, such as statins and peroxisome proliferator-activated receptor-agonists, may provide unexpected benefits for COPD patients. Treatment of COPD inflammation may concomitantly treat systemic inflammation and associated comorbidities. However, new broad-spectrum anti-inflammatory treatments, such as phosphodiesterase 4 inhibitors, have significant side-effects so it may be necessary to develop inhaled drugs in the future. Another approach is the reversal of corticosteroid resistance, for example with effective antioxidants. More research is needed on COPD comorbidities and their treatment.

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Section: Mechanismsmentioning

confidence: 99%

Section: Pde4 Inhibitorsmentioning

confidence: 99%

Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

European Respiratory Journal

1,465

1,113

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“…Interestingly, the gene expression of NFκB at 2 days in the inflammation group was also unexpectedly reduced in our study. A previous study also reported a reduction in this pro-inflammatory factor in muscle disuse due to immobilization 21 , but the significance of this reduction has not been clarified in the literature to date. Regarding these unexpected findings involving myostatin and NFkB expressions, a previous study showed a relationship between myostatin, TNF-α, and NFkB 41 .…”

Section: Muscle Response To Joint Inflammationmentioning

confidence: 90%

“…MAFbx (also known as atrogin-1) and Muscle Ring Finger-1 (MuRF1) [13][14][15][16] . Muscle fiber CSA reduction is also followed by changes in the regulation of genes related to muscle differentiation and growth (MyoD) 17,18 mass regulation (myostatin) 19 and proinflammatory factors, such as p38 Mitogen-Activated Protein Kinase (p38MAPK), Nuclear Factor kappa B-dependent (NFκB), and Tumour Necrosis Factoralpha (TNF-alpha) [20][21][22] . According to a previous study, the carrageenan injection increases TNF-alpha 23 , a cytokine able to increase the gene expression of MuRF1 and atrogin-1 in rat skeletal muscle 20,24,25 through the NFκB 20 and MAPK 25 pathways, respectively.…”

Section: Introductionmentioning

confidence: 99%

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle

Ramírez¹,

Russo²,

Delfino³

et al. 2013

Braz. J. Phys. Ther.

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| Background: Joint inflammation is a common clinical problem in patients treated by physical therapists. The hypothesis of this study is that joint inflammation induces molecular and structural changes in the soleus muscle, which is composed mainly of slow-twitch muscle fibers. Objective: To study the effect of tibiotarsal joint inflammation on muscle fiber cross-sectional area (CSA), gene expression levels (atrogin-1, MuRF1, MyoD, myostatin, p38MAPK, NFκB, TNF-alpha), and TNF-alpha protein in the soleus muscle. Method: Wistar rats were randomly divided into 3 periods (2, 7 and 15 days) and assigned to 4 groups (control, sham, inflammation, and immobilization). Results: In the inflammation group at 2 days, MuRF1 and p38MAPK expression had increased, and NFκB mRNA levels had decreased. At 7 days, myostatin expression had decreased. At 7 and 15 days, this group had muscle fiber CSA reduction. At 2 days, the immobilization group showed increased atrogin-1, MuRF1, NFκB, MyoD, and p38MAPK expressions and reduced muscle fiber CSA. At 7 and 15 days, myostatin mRNA levels had increased, and the CSA had decreased. The sham group showed increased p38MAPK and myostatin expressions at 2 and 7 days, respectively. No changes occurred in TNF-alpha gene or protein expression. Conclusion: Acute joint inflammation induces gene expression related to the proteolytic pathway without reduction in muscle fiber CSA. Chronic joint inflammation induced muscle atrophy without up-regulation of important genes belonging to the proteolytic pathway. Thus, muscle adaptation may differ according to the stage of joint inflammation, which suggests that the therapeutic modalities used by physical therapists at each stage should also be different.Keywords: skeletal muscle; joint disease; gene expression; muscle plasticity; physical therapy; rehabilitation. HOW TO CITE THIS ARTICLERamírez C, Russo TL, Delfino G, Peviani SM, Alcântara C, Salvini TF. Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle. Braz J Phys Ther. 2013 May-June; 17(3):244-254. http://dx

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“…Inflammation and oxidative stress are associated with skeletal muscle wasting in various disease states including cancer cachexia, muscular dystrophy, AIDS, sepsis, diabetes, chronic obstructive pulmonary disease (COPD), and cystic fibrosis [5][6][7][8][9]. Muscle wasting occurs as a result of a reduction in protein synthesis, an increase in protein degradation, or both [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Untitled

2014

JNHFE

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Nuclear factor-kappa B signaling in skeletal muscle atrophy

Cited by 372 publications

References 101 publications

Systemic manifestations and comorbidities of COPD

Systemic manifestations and comorbidities of COPD

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle

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