Aging and Lung Disease: A Clinical Guide

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It is caused by cigarette smoking and associated with inhalation of smoke and dust [4]. COPD is considered a severe health problem since it is one of the most important causes of morbidity and mortality in the United States and in developed countries. Additionally, by it is expected to be the 7th cause of death worldwide, representing over 4.

The most frequently described comorbidities include skeletal muscle waste, cachexia, pulmonary hypertension, lung cancer, congestive heart failure, ischemic heart disease, hyperlipidemia, normocytic anemia, diabetes, metabolic syndrome, osteoporosis, obstructive sleep apnea, depression, and arthritis [9,10]. COPD generally manifests at older ages, but there is evidence that events early in life, including exposure to noxious stimuli in the uterus may have long-term effects on lung health contributing to impaired lung function when older [11].

This disease among older adults is associated with a poor prognosis, usual hospitalization and increased mortality rate. However, age-related mechanisms causing emphysema are not clear [12]. The present review aims to describe emphysema and age-related factors that might influence on its development. An emphysematous lung presents airways inflammation, increased production of mucus and mild to severe pulmonary hypertension, causing air obstruction [14,16,17]. However, symptoms may vary depending on how advanced is the disease: individuals with mild emphysema commonly do not present symptoms at quiet breathing.

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In case of advanced disease, patients present barrel-shaped chest, weight loss, productive and chronic cough with or without sputum production, increased shortness of breath and constant use of breathing accessory muscles, poor exercise tolerance, and wheezing to respiratory failure or cor pulmonale [14,18,19]. The clearest signs of emphysema are seen in chest radiography which shows signs of hyperlucent lungs, reduced diffusion capacity and hyperinflation of the lungs [13,18].

However, Lee et al. Computed tomography CT of the thorax can be also a diagnosis tool to detect the disease at an early stage. Incidental CT findings of emphysema and airway thickening, seen on routine diagnostic CT scans, performed for nonpulmonary clinical symptoms, may help find probable patients with COPD [20].

Guest [13] also describes the difficulty in identifying emphysema, since it is usually correlated with other diseases. For example, asthma and chronic bronchitis also lead to airway obstruction. This confusion of diseases and symptoms may delay emphysema diagnoses and compromise treatment [13]. An effective way to diagnose this disease might be performing a lung function test.

The most efficient measure is the forced expiratory volume in one second FEV 1 [18]. However, Guest [13] claim that the test cannot provide a clear emphysema diagnosis because the same results are expected for other airway obstruction diseases. Consequently, emphysema might be clinically underdiagnosed, especially in older adults, who have usually association of chronic conditions, overlapping symptoms and difficulty in understanding respiratory function evaluation test [21].

Spirometry should not be used to screen airflow obstruction in individuals without respiratory symptoms [19]. This update indicates that the best variable for identifying adults with airflow obstruction is a smoking history greater than 40 pack-year. A combination of findings is more helpful for diagnosing airflow obstruction than is any individual sign, symptom, or piece of historical information.

The combination of all 3 of the following items—patient-reported smoking history greater than 55 pack-year, wheezing on auscultation; and patient self-reported wheezing—almost confirms the presence of airflow obstruction. In addition, the absence of all 3 items practically rules out airflow obstruction [19]. Different causes, and its interactions, are considered in the development of emphysema. Among them, better understood are inflammatory reactions of cells, mainly related to toxic exposure, such as tobacco. Others, for example apoptosis, are still under investigation [23].


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Karrasch et al. Rodrigues et al. There is wide evidence of shared features between pulmonary emphysema and aging lung With aging the respiratory system undergoes many changes in its structure and function resulting from interaction between individuals and environmental stresses. However, how the aging process contributes to the development of emphysema must be better understood [12,17].

The most important age-related change associated with emphysema might be the reduction in alveolar structures [24]. The cellular equivalent of aging is senescence, which is characterized by a nonproliferative state in which cells are metabolically active and apoptosis-resistant. Several molecular and cellular mechanisms are associated with cellular senescence including accumulation of DNA damage, impairment of DNA repair epigenetic modifications in nuclear DNA, protein damage from oxidative stress, and telomere attrition [3,26].

COPD following smoking is a disease-related senescence it causes DNA damage from compounds present in cigarettes that leads to telomere shortening, due to a greater need for repair on airway epithelium, after being injured by toxic substances. DNA damage and telomere shortening happen during healthy aging, but in smoking, the intensity of the stress is faster. Most of impairments in this disease occurs in the lung, thus smoking-induced senescent cells are probably located there [27].

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Telomere shortening, related to cell senescence, might help in the development of emphysema in older adults [12]. According to Karrasch et al. In addition, reduced length of telomere is related to dysfunctions in the immune system, which can lead to impairments in one organ. Telomere lengths are not entirely genetically inherited, accelerated telomeric loss can happen because of different environmental factors such as genotoxicity, air pollution and tobacco exposure [28].

Research has shown that telomeres are shorter in individuals with emphysema compared to non-smokers with the same age Albrecht et al. It is important to consider that the lungs are constantly exposed to pollutants and sometimes to inflammatory processes and oxidants, which might alter lung properties requiring constant repair. Reactive oxygen species ROS and other free radicals may damage cell membranes, particularly because of the oxidation of lipids, proteins and DNA. As a long-term result, with aging, this continuous remodeling can no longer be done, favoring the occurrence of diseases such as emphysema Apart from telomere shortening, the reduced ability of the alveolar tissue to repair can be attributed to lipofuscin, which was found in emphysematous lungs [12].

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Also, the production of oxygen-derived free radicals is increased, inducing aging of the lungs and activation of multiple genes responsible to encode pro-inflammatory molecules [17]. Telomere dysfunction is influenced by age, but also by external factors, such as psychological stress and oxidative stress, the last caused by smoking [24].

Cigarette smoking and aging are related to oxidative stress, which increases cell apoptosis. This phenomenon was found to be associated with increased levels of destruction of alveoli walls in individuals with emphysema [17,23].

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Smoking is also related to chronic inflammation of the airways, which is crucial to the development of emphysema. Most of the diseases affecting older adults are related to some kind of inflammation and persistent increase in the proinflammatory cytokines IL-6 and IL-8, shown to be induced by cigarette smoke and present in increased levels in lungs of individuals with COPD, are also triggered by aging [26].

In the case of emphysema, there is a higher circulation of inflammatory cells or specific concentration of pro-inflammatory cytokines. Another possible cause for emphysema is an imbalance between proteases and antiproteases. This situation can promote cell dysfunctions regarding their maintenance ability. In addition, proteases can destroy lung intercellular matrix, leading to apoptosis [30]. Research conducted by Tsuji et al. Inflammation can be triggered and amplified by alveolar injury, including either enhanced alveolar cell apoptosis or defective apoptotic cell clearance [26,32,33].


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Recent data from animal models of COPD as well as from studies in human beings suggest that another mechanism might be involved in the pathogenesis of COPD: disruption of the balance between apoptosis and replenishment of structural cells in the lung might contribute to the destruction of lung tissue in response to cigarette smoke, leading to emphysema. More studies are needed to identify the most important apoptotic pathway and the caspases involved in the development of COPD. Moreover, research is needed to clarify if apoptosis can be used as a therapeutic target to prevent further deterioration of the disease, which occurs even after the patients have quit smoking.

Finally, as disturbance of the balance between apoptosis and regeneration of structural lung cells seems important in the destruction of healthy lung tissue, it would be interesting to evaluate the potential use of stem cell therapy for emphysema [34,35]. Genetically modified mice have helped to identify factors underlying emphysema [24]. Sato et al. Hence, age might have great influence in the development of emphysema [30].

Onodera et al. This protein is an anti-ageing factor that is reduced at the plasma and lungs of COPD patients and is significantly correlated with disease severity. GDF11 showed anti-senescent effects in lung cells on both models. These findings suggest that GDF11 may have a part in the senescence observed in these patients, and that may be a future perspective in elucidating the mechanisms of cellular senescence in COPD. Causes of emphysema and how age contributes to its development still need to be clarified.

The use of rodents to investigate the morphology of pulmonary emphysema might be a possible model of research [15], which might help in the development of more effective treatments. As a consequence of the lack of knowledge in the fundamental cause of pulmonary emphysema, treatments are available to reduce symptoms, but none of them can stop the disease progression and decrease mortality rates yet. Research has been carried out and there are some innovations in medicine that might be efficient against this devastating disease [17].

Treatments for emphysema, especially when it is smoke related, comprehend the use of bronchodilators, supplemental oxygen for hypoxemia, non-invasive ventilation, exercise for pulmonary rehabilitation, prevention for secondary diseases and, when indicated, lung transplantation especially in patients younger than 60 years old [18,37,38]. Pharmacological treatments may reduce symptoms, risk and severity of exacerbations, improve overall health status and exercise capacity [5]. Long-term administration of oxygen increase survival in patients with severe resting hypoxemia, but it does not lengthen time to death or first hospitalization or provide sustained benefit for any of the measured outcomes in patients with stable COPD [39].

The mechanism in which oxygen works is based on reducing dyspnea and the respiratory rate while exercise, promoting a more efficient exhalation [16]. Pulmonary rehabilitation is a useful intervention to control symptoms and improve functional capacity in individuals with emphysema. Ries et al. This intervention improves ventilation-perfusion mismatch and cardiopulmonary hemodynamics, improving ventilatory mechanics by decreasing hyperinflation, elastic recoil and airway tethering, increasing respiratory muscle efficiency and survival rates, consequently promoting quality of life and improved exercise capacity.

Stolk et al. Although treatments with BM-MSCs are showing optimistic results in different lung disorders, including emphysema, showing a decrease in tissue destruction in elastase-induced emphysema, through secretion of paracrine factors such as epidermal growth factor [44], the use of MSCs are not fully understood. This new treatment modality for COPD patients is currently tested on clinical trials, varying in distinct stages of COPD, route of injection, type and dosage of cells, and outcomes [45]. MSCs show profound suppressive effects on immune cells and pathways, recent studies have indicated that MSCs suppress lung injury and inflammation in mouse models of inflammatory and immune mediated lung diseases [46].