Abnormal Lung Aging in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

被引:207
作者
Faner, Rosa [2 ,3 ]
Rojas, Mauricio [4 ]
MacNee, William [5 ]
Agusti, Alvar [1 ,2 ,3 ,6 ]
机构
[1] Univ Barcelona, Hosp Clin, Inst Torax, E-08036 Barcelona, Spain
[2] Fdn Invest Sanitaria Illes Balears, Ctr Invest Biomed Red Enfermedades Resp CIBERES, Palma De Mallorca, Spain
[3] Inst Invest Biomed August Pi & Sunyer IDIBAPS, Barcelona, Spain
[4] Univ Pittsburgh, Sch Med, Dorothy P & Richard P Simmons Ctr Interstitial Lu, Div Pulm Allergy & Crit Care Med,McGowan Inst Reg, Pittsburgh, PA USA
[5] Univ Edinburgh, Queens Med Res Inst, Edinburgh, Midlothian, Scotland
[6] CIBERES, IDIBAPS, Barcelona, Spain
关键词
chronic obstructive pulmonary disease; fibrosis; interstitial lung disease; inflammation; repair; GLYCATION END-PRODUCTS; MESENCHYMAL STEM-CELLS; AGE-RELATED-CHANGES; NF-KAPPA-B; BONE-MARROW; OXIDATIVE STRESS; T-CELLS; CIRCULATING FIBROCYTES; TELOMERE LENGTH; DENDRITIC CELLS;
D O I
10.1164/rccm.201202-0282PP
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Aging is a natural process characterized by progressive functional impairment and reduced capacity to respond appropriately to environmental stimuli and injury. The incidence of two common chronic respiratory diseases (chronic obstructive pulmonary disease [COPD] and idiopathic pulmonary fibrosis [IPF]) increases with advanced age. It is plausible, therefore, that abnormal regulation of the mechanisms of normal aging may contribute to the pathobiology of both COPD and IPF. This review discusses the available evidence supporting a number of aging mechanisms, including oxidative stress, telomere length regulation, cellular and immunosenescence, as well as changes in a number of antiaging molecules and the extracellular matrix, which are abnormal in COPD and/or IPF. A better understanding of these abnormalities may help in the design of novel and better therapeutic interventions for these patients.
引用
收藏
页码:306 / 313
页数:8
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