Cellular Senescence in the Lung Across the Age Spectrum.

Cellular Senescence in the Lung Across the Age Spectrum.

Am J Physiol Lung Cell Mol Physiol. 2019 Feb 20;:

Authors: Parikh P, Wicher S, Khandalavala K, Pabelick CM, Britt RD, Prakash YS

Abstract
Cellular senescence results in cell cycle arrest with secretion of cytokines, chemokines, growth factors and remodeling proteins (senescence associated secretory phenotype; SASP) that have autocrine and paracrine effects on the tissue microenvironment. SASP can promote remodeling, inflammation, infectious susceptibility, angiogenesis and proliferation, while hindering tissue repair and regeneration. While the role of senescence and contributions of senescent cells are increasingly recognized in the context of aging and a variety of disease states, relatively less is known regarding the portfolio and influences of senescent cells in normal lung growth and aging per se, or in the induction or progression of lung diseases across the age spectrum such as bronchopulmonary dysplasia, asthma, COPD, or pulmonary fibrosis. In this review, we introduce concepts of cellular senescence, the mechanisms involved in the induction of senescence, and the SASP portfolio that are relevant to lung cells, presenting the potential contribution of senescent cells and SASP to inflammation, hypercontractility and remodeling/fibrosis: aspects critical to a range of lung diseases. The potential to blunt lung disease by targeting senescent cells using a novel class of drugs (senolytics) is discussed. Potential areas for future research on cellular senescence in the lung are identified.

PMID: 30785345 [PubMed - as supplied by publisher]

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