title: Telomere Dysfunction and Cell Senescence in Chronic Lung Diseases: Therapeutic Potential.
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.
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France. Electronic address: serge.adnot@inserm.fr.
authors.forename: Serge
authors.initials: S
authors.lastname: Adnot
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Valérie
authors.initials: V
authors.lastname: Amsellem
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Laurent
authors.initials: L
authors.lastname: Boyer
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Marcos
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Mirna
authors.initials: M
authors.lastname: Saker
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Amal
authors.initials: A
authors.lastname: Houssaini
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Kanny
authors.initials: K
authors.lastname: Kebe
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Maylis
authors.initials: M
authors.lastname: Dagouassat
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Larissa
authors.initials: L
authors.lastname: Lipskaia
authors.affiliation: INSERM U955 and Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, 94010, Créteil, France; Université Paris-Est Créteil (UPEC), France.
authors.forename: Jorge
authors.initials: J
authors.lastname: Boczkowski
mesh_terms: D000818:Animals; D016922:Cellular Senescence / Q000187:drug effects*; D006801:Humans; D008171:Lung Diseases / Q000188:drug therapy* / Q000473:pathology*; D058990:Molecular Targeted Therapy / Q000379:methods*; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000473:pathology; D016615:Telomere / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D059505:Telomere Homeostasis / Q000187:drug effects*
keywords: COPD; Cellular senescence; emphysema; lung disease; pulmonary hypertension