Format

Send to

Choose Destination
Ann Am Thorac Soc. 2017 Nov;14(Supplement_5):S383-S388. doi: 10.1513/AnnalsATS.201705-370AW.

Mitochondrial Dysfunction in Pulmonary Fibrosis.

Author information

1
Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.

Abstract

The aging of the human population has resulted in an unprecedented increase in the incidence and prevalence of age-related diseases, including those of the lung. Idiopathic pulmonary fibrosis is a disease of aging, and is characterized by a progressive decline in lung function and high mortality. Recent studies suggest that mitochondrial dysfunction, which can accompany aging phenotypes, may contribute to the pathogenesis of idiopathic pulmonary fibrosis. In this review, we explore current evidence for mitochondrial dysfunction in alveolar epithelial cells, fibroblasts, and immune cells that participate in the fibrotic process. Further, the fates of these cell populations and the potential to target mitochondrial dysfunction as a therapeutic strategy are discussed.

KEYWORDS:

aging; mitochondrial dysfunction; pulmonary fibrosis

PMID:
29161077
PMCID:
PMC5711275
DOI:
10.1513/AnnalsATS.201705-370AW
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center