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Am J Respir Cell Mol Biol. 2019 Apr 9. doi: 10.1165/rcmb.2018-0410TR. [Epub ahead of print]

Cellular Senescence: The Trojan Horse in Chronic Lung Diseases.

Author information

1
University of Pittsburgh, 6614, Aging Institute, Pittsburgh, Pennsylvania, United States.
2
University of Pittsburgh Department of Medicine, 199716, Pulmonary, Allergy, and Critical Care Medicine, Pittsburgh, Pennsylvania, United States.
3
Hospital Clinic, Servei de Pneumologia, Barcelona, Spain.
4
University of Pittsburgh, Department of Medicine, Pittsburgh, Pennsylvania, United States.
5
University of Pittsburgh, 6614, Medicine, Aging Institute, Division of Geriatrics, Pittsburgh, Pennsylvania, United States.
6
University of Pittsburgh, Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Pittsburgh, Pennsylvania, United States ; anamora@pitt.edu.

Abstract

Senescence is a cell-fate decision characterized by irreversible arrest of proliferation accompanied by senescence associated secretory phenotype (SASP). Traditionally, cellular senescence was recognized as a beneficial physiological mechanism during development, wound healing, and in tumor suppression. However, in recent years identification of negative consequences of cellular senescence has emerged, illuminating its role in several chronic pathologies. In this context, senescent cells persist or accumulate and have detrimental consequences. In this review, we discuss the possibility that in COPD, persistent senescence impairs wound healing in the lung characterized by secretion of pro-inflammatory SASP factors and exhaustion of progenitor cells. In contrast, in IPF, chronic senescence in alveolar epithelial cells exacerbates the accumulation of senescent fibroblasts along with production of extracellular matrix. We review how cellular senescence may contribute to lung disease pathology.

KEYWORDS:

COPD; IPF; Lung; SASP; Senescence

PMID:
30965013
DOI:
10.1165/rcmb.2018-0410TR

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