| Literature DB >> 26096607 |
Serge Adnot1, Valérie Amsellem2, Laurent Boyer2, Elisabeth Marcos2, Mirna Saker2, Amal Houssaini2, Kanny Kebe2, Maylis Dagouassat2, Larissa Lipskaia2, Jorge Boczkowski2.
Abstract
Cellular senescence--defined as a stable cell-cycle arrest combined with stereotyped phenotypic changes--might play a causal role in various lung diseases, including chronic obstructive pulmonary disease (COPD), which is predicted to become the third leading cause of death worldwide by 2020. COPD is characterized by slowly progressive airflow obstruction and emphysema due to destruction of the lung parenchyma and is often complicated by pulmonary hypertension (PH). No curative treatment is available. Senescent cells, which accumulate with age, are increased in lungs from patients with COPD and express a robust senescence-associated secretory phenotype (SASP), which is proinflammatory. The aim of this review is to show how senescent cells can drive the lung alterations seen in COPD, which mechanisms may be involved, and whether therapeutic interventions may slow or delay the in vitro cell-senescence process and in vivo lung alterations. Published by Elsevier Inc.Entities:
Keywords: COPD; Cellular senescence; emphysema; lung disease; pulmonary hypertension
Mesh:
Year: 2015 PMID: 26096607 DOI: 10.1016/j.pharmthera.2015.06.007
Source DB: PubMed Journal: Pharmacol Ther ISSN: 0163-7258 Impact factor: 12.310