FAM13A regulates cellular senescence marker p21 and mitochondrial reactive oxygen species production in airway epithelial cells-Reference-Cited by-同舟云学术

FAM13A regulates cellular senescence marker p21 and mitochondrial reactive oxygen species production in airway epithelial cells

Published:2023-10-01 Issue:4 Volume:325 Page:L460-L466
ISSN:1040-0605
Container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology
language:en
Short-container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology

Author:

Chen Qing¹²^ORCID,Vasse Gwenda F.¹²^ORCID,Nwozor Kingsley Okechukwu¹²,Bekker Nicolaas J.¹²^ORCID,van den Berge Maarten²³^ORCID,Brandsma Corry-Anke¹²^ORCID,de Vries Maaike¹⁴^ORCID,Heijink Irene H.¹²³^ORCID

Affiliation:

1. University of Groningen, University Medical Center Groningen, Department of Pathology and Medical Biology, Groningen, The Netherlands

2. University of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD (GRIAC), Groningen, The Netherlands

3. University of Groningen, University Medical Center Groningen, Department of Pulmonology, Groningen, The Netherlands

4. University of Groningen, University Medical Center Groningen, Department of Epidemiology, Groningen, The Netherlands

Abstract

To our knowledge, this is the first study investigating the role of the COPD susceptibility gene FAM13A in aging and cellular senescence. We found that FAM13A negatively regulates the expression of the cellular senescence marker P21 and mitochondrial ROS production in the airway epithelium. In this way, the lower expression of FAM13A observed upon aging may facilitate cellular senescence and potentially contribute to accelerated lung aging in COPD.

Funder

China Scholarship Council

Universitair Medisch Centrum Groningen

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajplung.00141.2023

Reference26 articles.

1. Senescence in COPD and Its Comorbidities

2. Accelerated ageing of the lung in COPD: new concepts

3. COPD as a Disease of Accelerated Lung Aging

4. Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease

5. Unbalanced oxidant-induced DNA damage and repair in COPD: a link towards lung cancer

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