scholarly journals Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease

2016 ◽  
Vol 311 (6) ◽  
pp. L1113-L1140 ◽  
Author(s):  
Y. S. Prakash
Keyword(s):  
Smooth Muscle ◽  
Cell Types ◽  
Structure And Function ◽  
Normal Lung ◽  
Future Research ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Health And Disease ◽  
Growth And Aging ◽  
And Function

Airway structure and function are key aspects of normal lung development, growth, and aging, as well as of lung responses to the environment and the pathophysiology of important diseases such as asthma, chronic obstructive pulmonary disease, and fibrosis. In this regard, the contributions of airway smooth muscle (ASM) are both functional, in the context of airway contractility and relaxation, as well as synthetic, involving production and modulation of extracellular components, modulation of the local immune environment, cellular contribution to airway structure, and, finally, interactions with other airway cell types such as epithelium, fibroblasts, and nerves. These ASM contributions are now found to be critical in airway hyperresponsiveness and remodeling that occur in lung diseases. This review emphasizes established and recent discoveries that underline the central role of ASM and sets the stage for future research toward understanding how ASM plays a central role by being both upstream and downstream in the many interactive processes that determine airway structure and function in health and disease.

scholarly journals Airway smooth muscle in airway reactivity and remodeling: what have we learned?

2013 ◽  
Vol 305 (12) ◽  
pp. L912-L933 ◽  
Author(s):  
Y. S. Prakash
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Cell Types ◽  
Structure And Function ◽  
Contractile Element ◽  
Future Research ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Novel Therapeutic Strategies ◽  
And Function

It is now established that airway smooth muscle (ASM) has roles in determining airway structure and function, well beyond that as the major contractile element. Indeed, changes in ASM function are central to the manifestation of allergic, inflammatory, and fibrotic airway diseases in both children and adults, as well as to airway responses to local and environmental exposures. Emerging evidence points to novel signaling mechanisms within ASM cells of different species that serve to control diverse features, including 1) [Ca2+]i contractility and relaxation, 2) cell proliferation and apoptosis, 3) production and modulation of extracellular components, and 4) release of pro- vs. anti-inflammatory mediators and factors that regulate immunity as well as the function of other airway cell types, such as epithelium, fibroblasts, and nerves. These diverse effects of ASM “activity” result in modulation of bronchoconstriction vs. bronchodilation relevant to airway hyperresponsiveness, airway thickening, and fibrosis that influence compliance. This perspective highlights recent discoveries that reveal the central role of ASM in this regard and helps set the stage for future research toward understanding the pathways regulating ASM and, in turn, the influence of ASM on airway structure and function. Such exploration is key to development of novel therapeutic strategies that influence the pathophysiology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis.

scholarly journals Cellular senescence in the lung across the age spectrum

2019 ◽  
Vol 316 (5) ◽  
pp. L826-L842 ◽  
Author(s):  
Pavan Parikh ◽  
Sarah Wicher ◽  
Karl Khandalavala ◽  
Christina M. Pabelick ◽  
Rodney D. Britt ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Lung Diseases ◽  
Normal Lung ◽  
Future Research ◽  
Chronic Obstructive ◽  
Potential Contribution ◽  
Obstructive Pulmonary Disease ◽  
Paracrine Effects ◽  
Tissue Repair And Regeneration ◽  
Growth And Aging

Cellular senescence results in cell cycle arrest with secretion of cytokines, chemokines, growth factors, and remodeling proteins (senescence-associated secretory phenotype; SASP) that have autocrine and paracrine effects on the tissue microenvironment. SASP can promote remodeling, inflammation, infectious susceptibility, angiogenesis, and proliferation, while hindering tissue repair and regeneration. While the role of senescence and the contributions of senescent cells are increasingly recognized in the context of aging and a variety of disease states, relatively less is known regarding the portfolio and influences of senescent cells in normal lung growth and aging per se or in the induction or progression of lung diseases across the age spectrum such as bronchopulmonary dysplasia, asthma, chronic obstructive pulmonary disease, or pulmonary fibrosis. In this review, we introduce concepts of cellular senescence, the mechanisms involved in the induction of senescence, and the SASP portfolio that are relevant to lung cells, presenting the potential contribution of senescent cells and SASP to inflammation, hypercontractility, and remodeling/fibrosis: aspects critical to a range of lung diseases. The potential to blunt lung disease by targeting senescent cells using a novel class of drugs (senolytics) is discussed. Potential areas for future research on cellular senescence in the lung are identified.

Brain Structure and Function in Chronic Obstructive Pulmonary Disease

2012 ◽  
Vol 186 (3) ◽  
pp. 240-245 ◽  
Author(s):  
James W. Dodd ◽  
Ai Wern Chung ◽  
Martin D. van den Broek ◽  
Thomas R. Barrick ◽  
Rebecca A. Charlton ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Brain Structure ◽  
Structure And Function ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Brain Structure And Function ◽  
And Function

scholarly journals Effect of Oxidative Stress on Diaphragm Dysfunction and Exercise Intervention in Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Bingzhi Zhang ◽  
Peijun Li ◽  
Jian Li ◽  
Xiaodan Liu ◽  
Weibing Wu
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Exercise Intervention ◽  
Structure And Function ◽  
Chronic Obstructive ◽  
Positive Role ◽  
Obstructive Pulmonary Disease ◽  
Diaphragm Dysfunction ◽  
And Function

Chronic obstructive pulmonary disease (COPD) can cause extrapulmonary injury such as diaphragm dysfunction. Oxidative stress is one of the main factors causing diaphragm dysfunction in COPD. Exercise plays a positive role in the prevention and treatment of diaphragm dysfunction in COPD, and the changes in diaphragm structure and function induced by exercise are closely related to the regulation of oxidative stress. Therefore, on the basis of the review of oxidative stress and the changes in diaphragm structure and function in COPD, this article analyzed the effects of exercise on oxidative stress and diaphragm dysfunction in COPD and explored the possible mechanism by which exercise improves oxidative stress. Studies have found that diaphragm dysfunction in COPD includes the decline of muscle strength, endurance, and activity. Oxidative stress mainly affects the structure and function of the diaphragm in COPD through protein oxidation, protease activation and calcium sensitivity reduction. The effects of exercise on oxidative stress level and diaphragm dysfunction may differ depending on the intensity, duration, and style of exercise. The mechanism of exercise on oxidative stress in the diaphragm of COPD may include improving antioxidant capacity, reducing oxidase activity and improving mitochondrial function.

scholarly journals State of cardiovascular system in employees with chronic obstructive pulmonary disease in combination with arterial hypertension in terms of exposure to toxic games

2021 ◽  
Vol 38 (1) ◽  
pp. 16-28
Author(s):  
L. A. Panacheva ◽  
L. A. Shpagina
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Arterial Hypertension ◽  
Cardiovascular System ◽  
Structure And Function ◽  
Chronic Obstructive ◽  
Length Of Service ◽  
Obstructive Pulmonary Disease ◽  
The Right ◽  
And Function ◽  
Large Vessels

Objective. Identification of the features of the cardiovascular system damage in chronic obstructive pulmonary disease (COPD) combined with arterial hypertension (AH) in workers exposed to toxic gases (TG). Materials and methods. 132 house painters and paint production workers of the Novosibirsk aviation enterprise were included in 3 strata and examined: I-COPD and TG; II-COPD in combination with AH when exposed to TG; III COPD in combination with AH without exposure to TG. Employees of all strata were divided by length of service less than 10 and more than 10 years. The selection of workers in groups was carried out by a continuous method. Results. The most pronounced changes on the ECG, regardless of the length of service, were observed in workers with COPD in combination with hypertension and contact with TG (levogram and metabolic changes in the myocardium). When exposed to TG for more than 10 years, hypertrophy of the left parts of the heart was also detected. Among workers with COPD in combination with hypertension exposed to TG, the indicators of average pulmonary artery pressure (APAP) and pulmonary vascular resistance (PVR) elevated with increasing work experience; changes in the structure and function of the right and left parts of the heart and signs of remodeling of large vessels were also revealed. The same workers showed more pronounced changes in the daily blood pressure profile (DBPP) of AP with the prevalence of Non-dippers and Night-pickers. Conclusions. Among workers suffering from comorbid pathology, with increasing duration of TG exposure over 10 years, there were observed the most pronounced ECG changes (deviation of electrical axis to the left, metabolic changes in the myocardium, hypertrophy of the left heart); increased APAP and PVR 1.21 and 1.10 times; changes in the structure and function of the right and left chambers of the heart, remodeling of large vessels; increase in the frequency of variants of the DBPP of Non-dippers and Night-pickers.

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