Muscle-Bone Crosstalk in Chronic Obstructive Pulmonary Disease

Zhang, Lijiao; Sun, Yongchang

doi:10.3389/fendo.2021.724911

Cited by 29 publications

(29 citation statements)

References 99 publications

(129 reference statements)

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“…A recent retrospective study also indicated that chair rising test maximum force and grip strength were positively correlated with cortical geometric and microarchitectural parameters at all measured sites ( 27 ). Moreover, accumulating evidence suggested that bone and muscle can secrete a variety of cytokines to modulate each other, including myostatin, irisin, interleukin 6, osteocalcin, RANKL, and osteoprotegerin ( 28 ). Notably, as muscle ages, pathophysiological processes in muscle function present as selective loss of fast motor neurons while progressive loss of skeletal muscle mass presents as atrophy of muscle fibers, loss of number of muscle fibers, and reduced number of satellite cells ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Osteoporosis and sarcopenia-related traits: A bi-directional Mendelian randomization study

Liu

Lei

et al. 2022

Front. Endocrinol.

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BackgroundWith the advancement of world population aging, age-related osteoporosis (OP) and sarcopenia (SP) impose enormous clinical and economic burden on society. Evidence from accumulating studies indicates that they mutually influence one another. However, an observational study may be affected by potential confounders. Meanwhile, a Mendelian randomization (MR) study can overcome these confounders to assess causality.ObjectivesThe aim of this study was to evaluate the causality between OP and SP, informing new strategies for prevention, diagnosis, and treatment of osteosarcopenia.MethodsInstrumental variables (IVs) at the genome‐wide significance level were obtained from published summary statistics, and the inverse variance weighted method and several other MR methods were conducted to evaluate the bi-directional causality between SP and OP. Myopia was analyzed as a negative control outcome to test the validity of IVs.ResultsFemoral neck bone mineral density (FN BMD), lumbar spine BMD (LS BMD), and forearm BMD (FA BMD) had a direct causal effect on appendicular lean mass (ALM) [FA BMD-related analysis: odds ratio (OR) = 1.028, 95% confidence interval (CI) = (1.008,1.049), p = 0.006; FN BMD-related analysis: OR (95% CI) = 1.131 (1.092,1.170), p = 3.18E-12; LS BMD-related analysis: OR (95% CI) = 1.080 (1.062,1.098), p = 2.86E-19]. ALM had a significant causal effect on LS BMD [OR (95% CI) = (1.033,1.147), p = 0.001]. There was no evidence for causal association between BMD and low grip strength.ConclusionsOP and SP might mutually have a significant causal effect on each other. Our results supported the idea that the patient with severe OP was more susceptible to lose ALM and severe ALM loss might reduce LS BMD.

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Section: Discussionmentioning

confidence: 99%

Osteoporosis and sarcopenia-related traits: A bi-directional Mendelian randomization study

Liu

Lei

et al. 2022

Front. Endocrinol.

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“…Increased IL-6 is also associated with muscle mass loss and bone loss. In addition, COPD patients exhibit an elevated MSTN in skeletal muscle, while the raised MSTN in the serum of COPD patients is negatively correlated with total muscle mass [ 128 , 129 ]. MSTN can inhibit myoblast proliferation and differentiation, and promote muscle atrophy, which functions as a potent negative regulator of skeletal muscle growth and development [ 129 , 130 ].…”

Section: Relationship Between Inflammation-related Diseases and Skele...mentioning

confidence: 99%

“…In addition, COPD patients exhibit an elevated MSTN in skeletal muscle, while the raised MSTN in the serum of COPD patients is negatively correlated with total muscle mass [ 128 , 129 ]. MSTN can inhibit myoblast proliferation and differentiation, and promote muscle atrophy, which functions as a potent negative regulator of skeletal muscle growth and development [ 129 , 130 ]. After MSTN binds to TGF-β receptor, it activates Smad2 and Smad3 and regulates the transcription of genes involved in the proliferation and differentiation of skeletal muscle precursor cells, as well as the transcription of MuRF1 and atrogin-1 in mature muscle fibers [ 131 ].…”

Section: Relationship Between Inflammation-related Diseases and Skele...mentioning

confidence: 99%

“…After MSTN binds to TGF-β receptor, it activates Smad2 and Smad3 and regulates the transcription of genes involved in the proliferation and differentiation of skeletal muscle precursor cells, as well as the transcription of MuRF1 and atrogin-1 in mature muscle fibers [ 131 ]. In addition, MSTN activates the NF-κB pathway and induces an ROS increase in skeletal muscle through the Smad3-NF-κB-TNF-α pathway to cause skeletal muscle atrophy, and inhibits the IGF-1/Akt-mTOR pathway to reduce protein synthesis [ 129 , 132 ]. In COPD patients, MSTN expression is dysregulated, and the overactivated MSTN-Smad2/3 pathway is associated with skeletal muscle dysfunction.…”

Section: Relationship Between Inflammation-related Diseases and Skele...mentioning

confidence: 99%

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Inflammation: Roles in Skeletal Muscle Atrophy

Chang

et al. 2022

Antioxidants

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Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in skeletal muscle atrophy is extremely complex and has not been fully elucidated, thus hindering the development of effective therapeutic drugs and preventive measures for skeletal muscle atrophy. In this review, we elaborate on protein degradation pathways, including the ubiquitin-proteasome system (UPS), the autophagy-lysosome pathway (ALP), the calpain and caspase pathways, the insulin growth factor 1/Akt protein synthesis pathway, myostatin, and muscle satellite cells, in the process of muscle atrophy. Under an inflammatory environment, various pro-inflammatory cytokines directly act on nuclear factor-κB, p38MAPK, and JAK/STAT pathways through the corresponding receptors, and then are involved in muscle atrophy. Inflammation can also indirectly trigger skeletal muscle atrophy by changing the metabolic state of other tissues or cells. This paper explores the changes in the hypothalamic-pituitary-adrenal axis and fat metabolism under inflammatory conditions as well as their effects on skeletal muscle. Moreover, this paper also reviews various signaling pathways related to muscle atrophy under inflammatory conditions, such as cachexia, sepsis, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, chronic kidney disease, and nerve injury. Finally, this paper summarizes anti-amyotrophic drugs and their therapeutic targets for inflammation in recent years. Overall, inflammation is a key factor causing skeletal muscle atrophy, and anti-inflammation might be an effective strategy for the treatment of skeletal muscle atrophy. Various inflammatory factors and their downstream pathways are considered promising targets for the treatment and prevention of skeletal muscle atrophy.

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“…Inflammatory mediators IL-2 and IFNγ were inversely correlated with bone metabolism in COPD ( Bon et al, 2010 ). Skeletal muscle dysfunction mediated by inflammation was also an important factor in COPD-induced osteoporosis ( Zhang and Sun, 2021 ). High expression of IL-6 in COPD patients disrupted muscle–bone crosstalk and inhibited the secretion of irisin from muscle, which was positive for bone formation.…”

Section: Introductionmentioning

confidence: 99%

Osteoporosis in Patients With Respiratory Diseases

Qiu

Zhou

2022

Front. Physiol.

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Climate change, environmental pollution, and virus epidemics have sharply increased the number of patients suffering from respiratory diseases in recent years. Prolonged periods of illness and drug use increase the occurrence of complications in these patients. Osteoporosis is the common bone metabolism disease with respiratory disturbance, which affects prognosis and increases mortality of patients. The problem of osteoporosis in patients with respiratory diseases needs more attention. In this review, we concluded the characteristics of osteoporosis in some respiratory diseases including COPD, asthma, COVID-19, tuberculosis, and lung cancer. We revealed that hypoxia was the common pathogenesis of osteoporosis secondary to respiratory diseases, with malnutrition and corticosteroid abuse driving the progression of osteoporosis. Hypoxia-induced ROS accumulation and activated HIF-1α lead to attenuated osteogenesis and enhanced osteoclastogenesis in patients with respiratory diseases. Tuberculosis and cancer also invaded bone tissue and reduced bone strength by direct infiltration. For the treatment of osteoporosis in respiratory patients, oral-optimized bisphosphonates were the best treatment modality. Vitamin D was a necessary supplement, both for calcium absorption in osteogenesis and for improvement of respiratory lesions. Reasonable adjustment of the dose and course of corticosteroids according to the etiology and condition of patients is beneficial to prevent the occurrence and development of osteoporosis. Additionally, HIF-1α was a potential target for the treatment of osteoporosis in respiratory patients, which could be activated under hypoxia condition and involved in the process of bone remodeling.

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Muscle-Bone Crosstalk in Chronic Obstructive Pulmonary Disease

Cited by 29 publications

References 99 publications

Osteoporosis and sarcopenia-related traits: A bi-directional Mendelian randomization study

Osteoporosis and sarcopenia-related traits: A bi-directional Mendelian randomization study

Inflammation: Roles in Skeletal Muscle Atrophy

Osteoporosis in Patients With Respiratory Diseases

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