Evolving concepts in the pathogenesis of chronic obstructive pulmonary disease

被引:53
作者
Shapiro, SD
机构
[1] Washington Univ, Sch Med, Div Pediat Allergy & Pulm Med, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, St Louis Childrens & Barnes Jewish Hosp, Dept Pediat, St Louis, MO USA
[3] Washington Univ, Sch Med, St Louis Childrens & Barnes Jewish Hosp, Dept Med, St Louis, MO USA
[4] Washington Univ, Sch Med, St Louis Childrens & Barnes Jewish Hosp, Dept Cell Biol & Physiol, St Louis, MO USA
关键词
D O I
10.1016/S0272-5231(05)70172-6
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
The study of the pathogenesis of chronic obstructive pulmonary disease (COPD) has a rich history in the pulmonary community and has led to significant understanding of elastases, extracellular matrix, and inflammation in the lung. Nevertheless, there remains little to offer patients with COPD. Fortunately, the revolution in molecular biology has allowed the re-examination and the extension of knowledge of these concepts. This article discusses the molecular response of the lung to cigarette smoke, ranging from inflammation to proteinase-release lung destruction, and impaired repair of lung structures.
引用
收藏
页码:621 / +
页数:13
相关论文
共 58 条
[1]   Medical progress: Chronic obstructive pulmonary disease. [J].
Barnes, PJ .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (04) :269-280
[2]   Mice lacking neutrophil elastase reveal impaired host defense against gram negative bacterial sepsis [J].
Belaaouaj, A ;
McCarthy, R ;
Baumann, M ;
Gao, ZM ;
Ley, TJ ;
Abraham, SN ;
Shapiro, SD .
NATURE MEDICINE, 1998, 4 (05) :615-618
[3]   Neutrophil granule proteins in bronchoalveolar lavage fluid from subjects with subclinical emphysema [J].
Betsuyaku, T ;
Nishimura, M ;
Takeyabu, K ;
Tanino, M ;
Venge, P ;
Xu, SY ;
Kawakami, Y .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (06) :1985-1991
[4]   THE FUNCTIONAL-ACTIVITY OF ALPHA-1-PROTEINASE INHIBITOR IN BRONCHOALVEOLAR LAVAGE FLUIDS FROM HEALTHY-HUMAN SMOKERS AND NON-SMOKERS [J].
BOUDIER, C ;
PELLETIER, A ;
PAULI, G ;
BIETH, JG .
CLINICA CHIMICA ACTA, 1983, 132 (03) :309-315
[5]   The pulmonary matrix, glycosaminoglycans and pulmonary emphysema [J].
Cantor, JO ;
Cerreta, JM ;
Armand, G ;
Osman, M ;
Turino, GM .
CONNECTIVE TISSUE RESEARCH, 1999, 40 (02) :97-104
[6]  
CELLI BR, 1995, AM J RESP CRIT CARE, V152, pS77
[7]   THE ROLE OF THIOL PROTEASES IN TISSUE-INJURY AND REMODELING [J].
CHAPMAN, HA ;
MUNGER, JS ;
SHI, GP .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (06) :S155-S159
[8]   IMMUNOLOCALIZATION OF ELASTASE IN HUMAN EMPHYSEMATOUS LUNGS [J].
DAMIANO, VV ;
TSANG, A ;
KUCICH, U ;
ABRAMS, WR ;
ROSENBLOOM, J ;
KIMBEL, P ;
FALLAHNEJAD, M ;
WEINBAUM, G .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 78 (02) :482-493
[9]   COLLAGENASE EXPRESSION IN THE LUNGS OF TRANSGENIC MICE CAUSES PULMONARY-EMPHYSEMA [J].
DARMIENTO, J ;
DALAL, SS ;
OKADA, Y ;
BERG, RA ;
CHADA, K .
CELL, 1992, 71 (06) :955-961
[10]   Acute cigarette smoke-induced connective tissue breakdown is mediated by neutrophils and prevented by α1-antitrypsin [J].
Dhami, R ;
Gilks, B ;
Xie, CS ;
Zay, K ;
Wright, JL ;
Churg, A .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2000, 22 (02) :244-252