TY - JOUR
T1 - Cellular senescence
T2 - The Trojan horse in chronic lung diseases
AU - Hamsanathan, Shruthi
AU - Alder, Jonathan K.
AU - Sellares, Jacobo
AU - Rojas, Mauricio
AU - Gurkar, Aditi U.
AU - Mora, Ana L.
N1 - Funding Information:
Supported by National Institutes of Health grants 1R01 HL131789-01 (A.L.M.), 1R01 HL123766-01 (M.R.), R00 AG049126 (A.U.G.), R00 HL113105 (J.K.A.), and R01 HL135062 (J.K.A.).
Funding Information:
Supported by National Institutes of Health grants 1R01 HL131789-01 (A.L.M.), 1R01 HL123766-01 (M.R.), R00 AG049126 (A.U.G.), R00 HL113105 (J.K.A.), and R01 HL135062 (J.K.A.)
Publisher Copyright:
Copyright © 2019 by the American Thoracic Society.
PY - 2019
Y1 - 2019
N2 - Senescence is a cell fate decision characterized by irreversible arrest of proliferation accompanied by a senescence-associated secretory phenotype. Traditionally, cellular senescence has been recognized as a beneficial physiological mechanism during development and wound healing and in tumor suppression.However, in recent years, evidence 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 chronic obstructive pulmonary disease, persistent senescence impairs wound healing in the lung caused by secretion of proinflammatory senescence-associated secretory phenotype factors and exhaustion of progenitor cells. In contrast, in idiopathic pulmonary fibrosis, chronic senescence in alveolar epithelial cells exacerbates the accumulation of senescent fibroblasts together with production of extracellular matrix. We review how cellular senescence may contribute to lung disease pathology.
AB - Senescence is a cell fate decision characterized by irreversible arrest of proliferation accompanied by a senescence-associated secretory phenotype. Traditionally, cellular senescence has been recognized as a beneficial physiological mechanism during development and wound healing and in tumor suppression.However, in recent years, evidence 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 chronic obstructive pulmonary disease, persistent senescence impairs wound healing in the lung caused by secretion of proinflammatory senescence-associated secretory phenotype factors and exhaustion of progenitor cells. In contrast, in idiopathic pulmonary fibrosis, chronic senescence in alveolar epithelial cells exacerbates the accumulation of senescent fibroblasts together with production of extracellular matrix. We review how cellular senescence may contribute to lung disease pathology.
KW - Chronic obstructive pulmonary disease
KW - Idiopathic pulmonary fibrosis
KW - Lung
KW - Senescence
KW - Senescence-associated secretory phenotype
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U2 - 10.1165/rcmb.2018-0410TR
DO - 10.1165/rcmb.2018-0410TR
M3 - Review article
C2 - 30965013
AN - SCOPUS:85068343147
VL - 61
SP - 21
EP - 30
JO - American Journal of Respiratory Cell and Molecular Biology
JF - American Journal of Respiratory Cell and Molecular Biology
SN - 1044-1549
IS - 1
ER -