scholarly journals Roles of Mesenchymal Cells in the Lung: From Lung Development to Chronic Obstructive Pulmonary Disease

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3467
Author(s):  
Amel Nasri ◽  
Florent Foisset ◽  
Engi Ahmed ◽  
Zakaria Lahmar ◽  
Isabelle Vachier ◽  
...  

Mesenchymal cells are an essential cell type because of their role in tissue support, their multilineage differentiation capacities and their potential clinical applications. They play a crucial role during lung development by interacting with airway epithelium, and also during lung regeneration and remodeling after injury. However, much less is known about their function in lung disease. In this review, we discuss the origins of mesenchymal cells during lung development, their crosstalk with the epithelium, and their role in lung diseases, particularly in chronic obstructive pulmonary disease.

2021 ◽  
pp. 55-68
Author(s):  
Vyacheslav S. Lotkov ◽  
Anton Vladimirovich Glazistov ◽  
Antonina G. Baykova ◽  
Marina Yuryevna Vostroknutova ◽  
Natalia E. Lavrentieva

The formation and progression of chronic dust bronchitis and chronic bronchitis of toxic-chemical etiology, chronic obstructive pulmonary disease is accompanied by an increase in the degree of ventilation disorders, echocardiographic signs of hypertrophy and dilatation of the right ventricle are formed, typical for chronic pulmonary heart disease. The progression of disturbances in the function of external respiration in dusty lung diseases leads to a decrease in myocardial contractility. The detection of hemodynamic disturbances at the early stages of the development of occupational lung diseases indicates the need for individual monitoring of the functional state of the cardiovascular system in the process of contact with industrial aerosols, especially in groups of workers with long-term exposure.


2019 ◽  
Vol 51 (3) ◽  
pp. 494-505 ◽  
Author(s):  
Phuwanat Sakornsakolpat ◽  
◽  
Dmitry Prokopenko ◽  
Maxime Lamontagne ◽  
Nicola F. Reeve ◽  
...  

2015 ◽  
Vol 45 (3) ◽  
pp. 807-827 ◽  
Author(s):  
Silke Meiners ◽  
Oliver Eickelberg ◽  
Melanie Königshoff

Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, “dysregulation of the extracellular matrix”, which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases.


2018 ◽  
Author(s):  
Phuwanat Sakornsakolpat ◽  
Dmitry Prokopenko ◽  
Maxime Lamontagne ◽  
Nicola F. Reeve ◽  
Anna L. Guyatt ◽  
...  

SummaryChronic obstructive pulmonary disease (COPD) is the leading cause of respiratory mortality worldwide. Genetic risk loci provide novel insights into disease pathogenesis. To broaden COPD genetic risk loci discovery and identify cell type and phenotype associations we performed a genome-wide association study in 35,735 cases and 222,076 controls from the UK Biobank and additional studies from the International COPD Genetics Consortium. We identified 82 loci with P value < 5×10−8; 47 were previously described in association with either COPD or population-based lung function. Of the remaining 35 novel loci, 13 were associated with lung function in 79,055 individuals from the SpiroMeta consortium. Using gene expression and regulation data, we identified enrichment for loci in lung tissue, smooth muscle and alveolar type II cells. We found 9 shared genomic regions between COPD and asthma and 5 between COPD and pulmonary fibrosis. COPD genetic risk loci clustered into groups of quantitative imaging features and comorbidity associations. Our analyses provide further support to the genetic susceptibility and heterogeneity of COPD.


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