Extract
COPD is an age-related condition that is linked to cellular senescence [1]. In COPD, contributors to cellular senescence include oxidative stress from environmental factors, such as cigarette smoking and persistent lung inflammation [2]. These factors can also augment replicative senescence, which is characterised by progressive telomere attrition, ultimately leading to cell cycle arrest and death. Patients with COPD have shorter telomeres [3] and faster rates of telomere attrition [4] compared to controls; however, the clinical impact of cellular or replicative senescence in COPD remains uncertain.
Abstract
Epigenetic blood biomarkers of cellular and replicative senescence may improve the clinical assessment of COPD patients, particularly for those at a higher risk of death https://bit.ly/3nEM7tp
Footnotes
Conflict of interest: A.I. Hernandez Cordero has nothing to disclose.
Conflict of interest: C.X. Yang has nothing to disclose.
Conflict of interest: S. Milne has nothing to disclose.
Conflict of interest: X. Li has nothing to disclose.
Conflict of interest: Z. Hollander reports funding from Genome Canada, Genome British Columbia, Genome Quebec, the Canadian Institutes of Health Research, PROOF Centre of Excellence, St. Paul's Hospital Foundation and Providence Health Care for the Rapid Transition Program (RTP) cohort included in the manuscript.
Conflict of interest: V. Chen reports funding from Genome Canada, Genome British Columbia, Genome Quebec, the Canadian Institutes of Health Research, PROOF Centre of Excellence, St. Paul's Hospital Foundation and Providence Health Care for the Rapid Transition Program (RTP) cohort included in the manuscript.
Conflict of interest: R. Ng reports funding from Genome Canada, Genome British Columbia, Genome Quebec, the Canadian Institutes of Health Research, PROOF Centre of Excellence, St. Paul's Hospital Foundation and Providence Health Care for the Rapid Transition Program (RTP) cohort included in the manuscript.
Conflict of interest: S.J. Tebbutt has nothing to disclose.
Conflict of interest: J.M. Leung reports research grant funding (to institution) from Canadian Institutes of Health Research, Michael Smith Foundation for Health Research, BC Lung Association and Genome BC, outside the scope of the current manuscript.
Conflict of interest: D.D. Sin declares grants from AstraZeneca for an investigator-initiated randomised controlled trial in COPD; consulting fees from Novaira for sitting on an advisory board for COPD; and honoraria for speaking engagements from AstraZeneca, Boehringer Ingelheim and Grifols, all in the 36 months prior to manuscript submission.
Support statement: Supported by Genome Canada, Genome British Columbia, Genome Quebec, Canadian Institutes of Health Research, Providence Health Care, St. Paul's Hospital Foundation, and Prevention of Organ Failure Centre. A.I. Hernandez Cordero and S. Milne are supported by MITACS and Providence Airway Centre. J.M. Leung is supported by the Michael Smith for Health Research Foundation Health Professional Investigator Award and the CIHR/AstraZeneca Early Career Investigator Award. R. Ng is a tier 1 Canada Research Chair, and D.D. Sin is a tier 1 Canada Research Chair in COPD and holds the De Lazzari Family Chair at the Centre for Heart Lung Innovation.
- Received July 5, 2021.
- Accepted September 9, 2021.
- Copyright ©The authors 2021. For reproduction rights and permissions contact permissions{at}ersnet.org