This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
Research Article
Sofia Pavanello
Occupational Medicine, Department of Cardiac, Thoracic, and Vascular Sciences and Public Health, University Hospital of Padua, Via Giustiniani, 2, 35128, Padova, Italy
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, shows striking clinical aging-associated features of lung. We tested the hypothesis that lung biological aging in COPD is accelerated. Biological aging was assessed by mitotic telomere length (TL) and non-mitotic age-dependent methylation changes in specific CpGs (DNAmAge) of lung cells, obtained from induced sputum, and peripheral blood leucocytes in 18 COPD patients (72.4±7.7 years; 50% males), clinically appraised by lung function and blood parameters. DNAmAge (67.4±5.80 vs 61.6±5.40 years; p=0.0003), AgeAcc (-4.5±5.02 vs -10.8±3.50 years; p=0.0003) and TL attrition (1.05±0.35 vs 1.48±0.21 T/S; p=0.0341) are higher in lung than blood in the same patients. Blood DNAmAge (r=0.927245; p=0.0026) and AgeAcc (r=0.916445; p=0.0037), but not TL, highly correlate with that of lung. Therefore, blood can be a proxy indicator of lung biological age. Multiple regression analyses show that both blood DNAmAge and AgeAcc decrease (i.e., younger) in patients with combined inhaled corticosteroids (ICS) therapy (p=0.0494 and p=0.0553) and FEV1% enhancement (p=0.0254; p=0.0296). In conclusion, the new finding, that lung of COPD patients is remarkably biologically older than blood, opens new research challenge on novel therapeutic approaches to counteract this key aspect of the disease.
Keywords
Chronic obstructive pulmonary disease, telomere length, DNA methylation age, age acceleration, epigenetic age, biological aging, induced sputum
Figure 1
The full text of this article is available to read as a PDF.
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 02 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiac & Cardiovascular Systems
Learn more about our company.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
Sofia Pavanello
Occupational Medicine, Department of Cardiac, Thoracic, and Vascular Sciences and Public Health, University Hospital of Padua, Via Giustiniani, 2, 35128, Padova, Italy
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 02 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiac & Cardiovascular Systems
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, shows striking clinical aging-associated features of lung. We tested the hypothesis that lung biological aging in COPD is accelerated. Biological aging was assessed by mitotic telomere length (TL) and non-mitotic age-dependent methylation changes in specific CpGs (DNAmAge) of lung cells, obtained from induced sputum, and peripheral blood leucocytes in 18 COPD patients (72.4±7.7 years; 50% males), clinically appraised by lung function and blood parameters. DNAmAge (67.4±5.80 vs 61.6±5.40 years; p=0.0003), AgeAcc (-4.5±5.02 vs -10.8±3.50 years; p=0.0003) and TL attrition (1.05±0.35 vs 1.48±0.21 T/S; p=0.0341) are higher in lung than blood in the same patients. Blood DNAmAge (r=0.927245; p=0.0026) and AgeAcc (r=0.916445; p=0.0037), but not TL, highly correlate with that of lung. Therefore, blood can be a proxy indicator of lung biological age. Multiple regression analyses show that both blood DNAmAge and AgeAcc decrease (i.e., younger) in patients with combined inhaled corticosteroids (ICS) therapy (p=0.0494 and p=0.0553) and FEV1% enhancement (p=0.0254; p=0.0296). In conclusion, the new finding, that lung of COPD patients is remarkably biologically older than blood, opens new research challenge on novel therapeutic approaches to counteract this key aspect of the disease.
Figure 1
The full text of this article is available to read as a PDF.
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
Loading...