Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis

Author:

Parimon Tanyalak1ORCID,Chen Peter1ORCID,Stripp Barry R.1ORCID,Liang Jiurong1,Jiang Dianhua1,Noble Paul W.1,Parks William C.1,Yao Changfu1

Affiliation:

1. Division of Pulmonary and Critical Care Medicine, Department of Medicine, Women’s Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States

Abstract

With an aging population, lung fibrotic diseases are becoming a global health burden. Dysfunctional repair of the alveolar epithelium is a key causative process that initiates lung fibrosis. Normal alveolar regeneration relies on functional progenitor cells; however, the senescence of these cells, which increases with age, hinders their ability to contribute to repair. Here, we discuss studies on the control and consequence of progenitor cell senescence in fibrosis and opportunities for research.

Funder

HHS | NIH | National Institute on Aging

Foundation for the National Institutes of Health

Francis Family Foundation

HHS | NIH | National Heart, Lung, and Blood Institute

UC | UCLA | Clinical and Translational Science Institute, University of California, Los Angeles

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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