COPD as a Disease of Accelerated Lung Aging

Ito, Kazuhiro; Barnes, Peter J.

doi:10.1378/chest.08-1419

Cited by 524 publications

(432 citation statements)

References 49 publications

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“…The molecular pathways of ageing are now much better understood and have revealed novel targets for therapeutic intervention, such as the anti-ageing molecules sirtuin 1 and peroxisome proliferator-activated-c coactivator 1a [214].…”

Section: Future Developmentsmentioning

confidence: 99%

Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

Eur Respir J

1,476

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: Future Developmentsmentioning

confidence: 99%

Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

Eur Respir J

1,476

1,113

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“…However, the mechanism of CS and COPD development is not fully understood and could be explained by different hypotheses including inflammation, protease-antiprotease imbalance, oxidant stress (3)(4)(5)(6), apoptosis (7), and accelerated lung aging (8). Among them, inflammation, oxidative stress, and protease-antiprotease imbalance have been suggested as a pathogenic triad in COPD (6).…”

Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

Lee

Jeong

et al. 2015

Journal of Biological Chemistry

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Background: Interaction between oxidative stress (CSE) and protease (NE) may contribute to COPD pathogenesis. Results: Although NE enhances CSE-induced IL-8, it suppresses VEGF production, which is due to degradation by uptake of NE into bronchial epithelial cells. Conclusion: NE contributes to the pathogenesis of COPD by enhancing inflammation and apoptosis.Significance: This provides a molecular mechanism for understanding COPD pathogenesis.

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“…Chronic obstructive pulmonary disease (COPD), lung cancer and idiopathic pulmonary fibrosis are lung diseases with an increase in incidence by age. In COPD, chronic inflammation and oxidative stress are among the generally accepted pathophysiological mechanisms but, as discussed for other degenerative diseases, accelerated ageing resulting in premature cell senescence may contribute to the pathobiology [7][8][9]. Although clinical and epidemiological studies provide some evidence for this hypothesis, the data base is still limited [8], so our study aimed to provide further clues on this.…”

Section: Introductionmentioning

confidence: 98%

Telomere length in circulating leukocytes is associated with lung function and disease

Albrecht¹,

Sillanpää²,

Karrasch³

et al. 2013

Eur Respir J

110

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Several clinical studies suggest the involvement of premature ageing processes in chronic obstructive pulmonary disease (COPD). Using an epidemiological approach, we studied whether accelerated ageing indicated by telomere length, a marker of biological age, is associated with COPD and asthma, and whether intrinsic age-related processes contribute to the interindividual variability of lung function.Our meta-analysis of 14 studies included 934 COPD cases with 15 846 controls defined according to the Global Lungs Initiative (GLI) criteria (or 1189 COPD cases according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria), 2834 asthma cases with 28 195 controls, and spirometric parameters (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) of 12 595 individuals. Associations with telomere length were tested by linear regression, adjusting for age, sex and smoking status.We observed negative associations between telomere length and asthma (b5 -0.0452, p50.024) as well as COPD (b5 -0.0982, p50.001), with associations being stronger and more significant when using GLI criteria than those of GOLD. In both diseases, effects were stronger in females than males. The investigation of spirometric indices showed positive associations between telomere length and FEV1 (p51.07610 -7 ), FVC (p52.07610 -5 ), and FEV1/FVC (p55.27610 -3 ). The effect was somewhat weaker in apparently healthy subjects than in COPD or asthma patients.Our results provide indirect evidence for the hypothesis that cellular senescence may contribute to the pathogenesis of COPD and asthma, and that lung function may reflect biological ageing primarily due to intrinsic processes, which are likely to be aggravated in lung diseases. @ERSpublicationsTelomere length is decreased in asthma and COPD patients and positively associated with spirometric indices

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COPD as a Disease of Accelerated Lung Aging

Cited by 524 publications

References 49 publications

Systemic manifestations and comorbidities of COPD

Systemic manifestations and comorbidities of COPD

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

Telomere length in circulating leukocytes is associated with lung function and disease

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