Treatment with long acting muscarinic antagonists stimulates serum levels of irisin in patients with COPD

Mandal, Jyotshna; Roth, Michael; Papakonstantinou, Eleni; Sun, Qingzhu; Costa, Luigi; Boeck, Lucas; Scherr, Andreas; Rakic, Janko; Louis, Renaud; Milenković, Branislava; Boersma, Wim; Κostikas, Κonstantinos; Blasi, Francesco; Aerts, Joachim; Rohde, Gernot; Lacoma, Alícia; Torres, Antoni; Welte, Tobias; Tamm, Michael; Stolz, Daiana

doi:10.1016/j.pupt.2017.10.011

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…Patients included in the PROMISE study had moderate to very severe COPD and were free of an exacerbation for at least 4 weeks before inclusion in the study. [12][13][14] After the baseline visit, patients had scheduled visits every 6 months and unscheduled visits at exacerbation and 4 weeks later. The median follow-up was 24 months.…”

Section: Study Design and Participantsmentioning

confidence: 99%

Ηeparan sulphate in infectious and non‐infectious exacerbations of COPD

et al. 2023

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Background and Objective Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are associated with worsening health outcomes and effective treatment of each episode is essential. In this study, we aimed to investigate if plasma levels of heparan sulphate (HS) are associated with the aetiology of AECOPD. Methods COPD patients (N = 1189), GOLD grade II–IV, from a discovery cohort (N = 638) and from a validation cohort (N = 551), were included in the study. HS and heparanase (HSPE‐1) were measured longitudinally in plasma at stable state, at AECOPD and at 4 weeks follow‐up. Results Plasma HS was higher in patients with COPD as compared with non‐COPD controls and was significantly increased at AECOPD as compared to stable state (p < 0.001) in the discovery and in the validation cohorts. Four distinct exacerbation groups were classified based on aetiology (no‐infection/bacterial‐infection/viral‐infection/bacterial and viral coinfection) in the validation cohort. The fold‐increase of HS from stable state to AECOPD was associated with the aetiology of exacerbation and was higher in cases with bacterial and viral coinfections. HSPE‐1 was also significantly increased at AECOPD, however, there was no association of HSPE‐1 levels with the aetiology of these events. The probability of having an infection at AECOPD was raised as HS levels increased from stable state to AECOPD. This probability was higher for bacterial infections than viral infections. Conclusion The results of our study indicate that circulating levels of HS are increased at AECOPD and this increase may be associated with the aetiology of these events.

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Section: Study Design and Participantsmentioning

confidence: 99%

Ηeparan sulphate in infectious and non‐infectious exacerbations of COPD

et al. 2023

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“…Ye et al reported that irisin increased mitochondrial autophagy and respiratory capacity in C2C12 skeletal muscle cells through the p38 mitogen-activated protein kinase pathway [61]. Mandal et al found that serum irisin levels were increased in patients with COPD after treatment with long-acting muscarinic antagonists and that the increased levels were positively correlated with the 6MWD [62]. These findings suggest that insufficient irisin secretion in the skeletal muscles of patients with COPD may hinder its protective effect on mitochondrial function by reducing P-MAPK levels, leading to decreased skeletal muscle exercise capacity and 6MWD.…”

Section: Myokines Affect Mitochondrial Functionmentioning

confidence: 99%

Revisiting Skeletal Muscle Dysfunction and Exercise in Chronic Obstructive Pulmonary Disease: Emerging Significance of Myokines

Han,

Li,

et al. 2023

Aging and disease

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Skeletal muscle dysfunction (SMD) is the most significant extrapulmonary complication and an independent prognostic indicator in patients with chronic obstructive pulmonary disease (COPD). Myokines, such as interleukin (IL)-6, IL-15, myostatin, irisin, and insulin-like growth factor (IGF)-1, play important roles in skeletal muscle mitochondrial function, protein synthesis and breakdown balance, and regeneration of skeletal muscles in COPD. As the main component of pulmonary rehabilitation, exercise can improve muscle strength, muscle endurance, and exercise capacity in patients with COPD, as well as improve the prognosis of SMD and COPD by regulating the expression levels of myokines. The mechanisms by which exercise regulates myokine levels are related to microRNAs. IGF-1 expression is upregulated by decreasing the expression of miR-1 or miR-29b. Myostatin downregulation and irisin upregulation are associated with increased miR-27a expression and decreased miR-696 expression, respectively. These findings suggest that myokines are potential targets for the prevention and treatment of SMD in COPD. A comprehensive analysis of the role and regulatory mechanisms of myokines can facilitate the development of new exercise-based therapeutic approaches for patients with COPD.

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“…For the validation cohort, we consecutively recruited 638 patients that, at baseline, appeared with clinically stable, moderate to very severe COPD (forced expiratory volume in 1 s (FEV1) % pred <80% and FEV1/forced vital capacity (FVC) ⩽0.7), based on physical examination and spirometry, at least 4 weeks after the latest exacerbation was resolved [19][20][21]. All patients were ⩾40 years old with a smoking history ⩾10 pack-years.…”

Section: Study Design and Participantsmentioning

confidence: 99%