Fibrogenic Reactions in Lung Disease

被引:92
作者
Araya, Jun [1 ]
Nishimura, Stephen L. [2 ]
机构
[1] Jikei Univ, Sch Med, Div Resp Dis, Dept Internal Med, Tokyo 1058461, Japan
[2] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94110 USA
基金
美国国家卫生研究院;
关键词
airway; asthma; emphysema; interstitial fibrosis; GROWTH-FACTOR-BETA; OBSTRUCTIVE PULMONARY-DISEASE; LATENT TGF-BETA; USUAL INTERSTITIAL PNEUMONIA; EPITHELIAL-MESENCHYMAL TRANSITION; SMALL AIRWAY DIMENSIONS; TRANSFORMING GROWTH-FACTOR-BETA-1; GENE-EXPRESSION; SMOOTH-MUSCLE; MYOFIBROBLAST DIFFERENTIATION;
D O I
10.1146/annurev.pathol.4.110807.092217
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Fibrogenic lung reactions occur as a common phenotype shared among disorders of heterogeneous etiologies. Even with a common etiology, the extent and pattern of fibrosis vary greatly among individuals, even within families, suggesting complex gene-environment interactions. The search for mechanisms shared among all fibrotic lung diseases would represent a major advance in the identification of therapeutic targets that could have a broad impact on lung health. Although it is difficult to grasp all of the complexities of the varied cell types and cytokine networks involved in lung fibrogenic responses, and to predict the biologic responses to the overexpression or deficiency of individual cytokines, a large body of evidence converges on a single common theme: the central importance of the transforming growth factor beta (TGF-beta) pathway. Therapies that act upstream or downstream of TGF-beta activation have the therapeutic potential to treat all fibrogenic responses in the lung.
引用
收藏
页码:77 / 98
页数:22
相关论文
共 132 条
[71]   The epithelial-mesenchymal transition generates cells with properties of stem cells [J].
Mani, Sendurai A. ;
Guo, Wenjun ;
Liao, Mai-Jing ;
Eaton, Elinor Ng. ;
Ayyanan, Ayyakkannu ;
Zhou, Alicia Y. ;
Brooks, Mary ;
Reinhard, Ferenc ;
Zhang, Cheng Cheng ;
Shipitsin, Michail ;
Campbell, Lauren L. ;
Polyak, Kornelia ;
Brisken, Cathrin ;
Yang, Jing ;
Weinberg, Robert A. .
CELL, 2008, 133 (04) :704-715
[72]   The logic of TGFβ signaling [J].
Massague, Joan ;
Gomis, Roger R. .
FEBS LETTERS, 2006, 580 (12) :2811-2820
[73]   SMALL AIRWAYS DISEASE IN PATIENTS WITHOUT CHRONIC AIR-FLOW LIMITATION [J].
MATSUBA, K ;
SHIRAKUSA, T ;
KUWANO, K ;
HAYASHI, S ;
SHIGEMATSU, N .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1987, 136 (05) :1106-1111
[74]   Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema [J].
Morris, DG ;
Huang, XZ ;
Kaminski, N ;
Wang, YN ;
Shapiro, SD ;
Dolganov, G ;
Glick, A ;
Sheppard, D .
NATURE, 2003, 422 (6928) :169-173
[75]   The integrin αvβ8 mediates epithelial homeostasis through MT1-MMP-dependent activation of TGF-β1 [J].
Mu, DZ ;
Cambier, S ;
Fjellbirkeland, L ;
Baron, JL ;
Munger, JS ;
Kawakatsu, H ;
Sheppard, D ;
Broaddus, VC ;
Nishimura, SL .
JOURNAL OF CELL BIOLOGY, 2002, 157 (03) :493-507
[76]   The integrin αvβ6 binds and activates latent TGFβ1:: A mechanism for regulating pulmonary inflammation and fibrosis [J].
Munger, JS ;
Huang, XZ ;
Kawakatsu, H ;
Griffiths, MJD ;
Dalton, SL ;
Wu, JF ;
Pittet, JF ;
Kaminski, N ;
Garat, C ;
Matthay, MA ;
Rifkin, DB ;
Sheppard, D .
CELL, 1999, 96 (03) :319-328
[77]   Expression of Smad7 in bronchial epithelial cells is inversely correlated to basement membrane thickness and airway hyperresponsiveness in patients with asthma [J].
Nakao, A ;
Sagara, H ;
Setoguchi, Y ;
Okada, T ;
Okumura, K ;
Ogawa, H ;
Fukuda, T .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2002, 110 (06) :873-878
[78]   PATHOLOGIC-CHANGES IN PERIPHERAL AIRWAYS OF YOUNG CIGARETTE SMOKERS [J].
NIEWOEHNER, DE ;
KLEINERMAN, J ;
RICE, DB .
NEW ENGLAND JOURNAL OF MEDICINE, 1974, 291 (15) :755-758
[79]  
NISHIMURA SL, 2005, MURRAY NADELS TXB RE, P407
[80]   A mutation in the surfactant protein C gene associated with familial interstitial lung disease. [J].
Nogee, LM ;
Dunbar, AE ;
Wert, SE ;
Askin, F ;
Hamvas, A ;
Whitsett, JA .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (08) :573-579