Sleep in chronic respiratory disease: COPD and hypoventilation disorders

McNicholas, Walter T.; Hansson, Daniel; Schiza, Sofia; Grote, Ludger

doi:10.1183/16000617.0064-2019

Cited by 95 publications

(68 citation statements)

References 133 publications

(145 reference statements)

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“…COPD is a progressive lung disease often caused by smoking; it is characterized by pulmonary emphysema, bronchitis, and fibrosis, and it induces tissue injury and airflow obstruction. 12 Pulmonary emphysema is an abnormal and persistent dilation in the distal air space of the terminal bronchiole in the lung. It is accompanied by destruction of the alveolar wall and bronchiole with no obvious pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter

Zhang

Wang

et al. 2020

J Int Med Res

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Objective Many lung diseases are associated with changes in autophagic activity. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway plays a key regulatory role in autophagy. Our aim was to explore the function of PI3K/AKT/mTOR pathway on autophagy in chronic obstructive pulmonary disease (COPD) caused by particulate matter with a diameter <2.5 µm (PM2.5). Methods Male C57BL/6 mice were randomly divided into sham, model, and PI3K inhibitor groups. Mice were exposed to PM2.5 for 4 weeks to establish an in vivo COPD model. Alveolar epithelial cells were stimulated with PM2.5 to establish an in vitro COPD model. Results In mice with COPD induced by PM2.5, the PI3K inhibitor PF-04979064 suppressed protein expression of PI3K, p-AKT, and p-mTOR to increase apoptosis of alveolar epithelial cells and reduce autophagy. Short interfering PI3K suppressed the PI3K/AKT/mTOR pathway to induce apoptosis and reduce autophagy of alveolar epithelial cells in an in vitro model of COPD. Activation of PI3K induced the PI3K/AKT/mTOR pathway to reduce apoptosis of alveolar epithelial cells in the in vitro model of COPD by promoting autophagy. Conclusions These data demonstrate that PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in COPD.

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Section: Discussionmentioning

confidence: 99%

The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter

Zhang

Wang

et al. 2020

J Int Med Res

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“…But for the patient suffering from poor sleep, the course of treatment is unclear. Diagnosis of OSA and sleep disorders in COPD requires specialist clinical experience to recognize distinct phenotypes that predispose to these comorbidities and provide effective management for the future 67 . Leg cramps are a further common symptom in COPD which can disturb sleep, but for which treatment options are limited 68 …”

Section: Addressing the Burden Of Copdmentioning

confidence: 99%

Contemporary perspectives in COPD: Patient burden, the role of gender and trajectories of multimorbidity

et al. 2021

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An individual's experience of COPD is determined by many factors in addition to the pathological features of chronic bronchitis and emphysema and the symptoms that derive directly from them. Multimorbidity is the norm rather than the exception, so most people with COPD are living with a range of other medical problems which can decrease overall quality of life. COPD is caused by the inhalation of noxious particles or gases, in particular tobacco smoke, but also by early life disadvantage impairing lung development and by occupations where inhaled exposures are common (e.g. industrial, farming and cleaning work). Wealthy people are therefore relatively protected from developing COPD and people who do develop the condition may have reduced resources to cope. COPD is also no longer a condition that predominantly affects men. The prevalence of COPD among women has equalled that of men since 2008 in many high‐income countries, due to increased exposure to tobacco, and in low‐income countries due to biomass fuels. COPD is one of the leading causes of death in women in the USA, and death rates attributed to COPD in women in some countries are predicted to overtake those of men in the next decade. Many factors contribute to this phenomenon, but in addition to socioeconomic and occupational factors, there is increasing evidence of a higher susceptibility of females to smoking and pollutants. Quality of life is also more significantly impaired in women. Although most medications (bronchodilators and inhaled corticosteroids) used to treat COPD demonstrate similar trends for exacerbation prevention and lung function improvement in men and women, this is an understudied area and clinical trials frequently have a preponderance of males. A better understanding of gender‐based predictors of efficacy of all therapeutic interventions is crucial for comprehensive patient care. There is an urgent need to recognize the increasing burden of COPD in women and to facilitate global improvements in disease prevention and management in this specific population. Many individuals with COPD follow a trajectory of both lung function decline and also multimorbidity. Unfavourable lung function trajectories throughout life have implications for later development of other chronic diseases. An enhanced understanding of the temporal associations underlying the development of coexisting diseases is a crucial first step in unravelling potential common disease pathways. Lessons can be learned from exploring disease trajectories of other NCD as well as multimorbidity development. Further research will be essential to explain how early life risk factors commonly influence trajectories of COPD and other diseases, how different diseases develop in relation to each other in a temporal way and how this ultimately leads to different multimorbidity patterns in COPD. This review integrates new knowledge and ideas pertaining to three broad themes (i) the overall burden of disease in COPD, (ii) an unappreciated high burden in women and (iii) the contrast...

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“…In REM sleep, respiratory muscle function is reduced, during which diaphragm contraction is preserved, and minute ventilation can decrease more than 15% in this phase of sleep in normal individuals 50 . This decrease of respiratory muscle function in patients with lung disease is more pronounced, 11 and furthermore, patients with hyperinflation have decreased diaphragm contraction 4,51 . A decrease in minute ventilation while asleep can lead to hypercapnia.…”

Section: Sbd: Screening Tools and Definition Of Key Termsmentioning

confidence: 99%

“…Untreated SDB can adversely affect outcomes in patients with chronic lung disease, 11 and therefore it is essential that CF clinicians expeditiously screen, diagnose, and treat SDB in the CF population. In this review, we focus on three clinically relevant categories of SBD: nocturnal hypoxemia, OSA, and nocturnal hypoventilation.…”

Section: Introductionmentioning

confidence: 99%

Sleep‐disordered breathing in cystic fibrosis

Jagpal

Jobanputra

Ahmed

et al. 2021

Pediatric Pulmonology

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Sleep‐disordered breathing (SDB) is an under recognized comorbidity in the cystic fibrosis (CF) population across the lifespan. Nocturnal hypoxemia, obstructive sleep apnea, and nocturnal hypoventilation are respiratory abnormalities that occur commonly during sleep in patients with lung disease, and have deleterious consequences to the quality of life in people with CF. Effective screening for these abnormalities is needed to allow for timely initiation of treatment, which has been reported to be efficacious. Lack of treatment leads to worsened pulmonary, cardiovascular, and metabolic outcomes in patients. In this review, we give an overview of SDB for the CF clinician, including prevalence, treatment, and suggestions for future research. We strongly encourage the CF community to incorporate evaluation for SDB in CF clinical care so that outcomes for the subset of the CF patients with comorbid SDB improve.

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Sleep in chronic respiratory disease: COPD and hypoventilation disorders

Cited by 95 publications

References 133 publications

The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter

The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter

Contemporary perspectives in COPD: Patient burden, the role of gender and trajectories of multimorbidity

Sleep‐disordered breathing in cystic fibrosis

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