|
 |
|
|||||||
|
|||||||||
© 2006 The American Thoracic Society
Matrix Metalloproteases in Aberrant Fibrotic Tissue Remodeling
Facultad de Ciencias, Universidad Nacional Autónoma de México; and Instituto Nacional de Enfermedades Respiratorias, Mexico DF, Mexico
Correspondence and requests for reprints should be addressed to Annie Pardo, Ph.D., Universidad Nacional Autónoma de México, Facultad de Ciencias, Ciudad Universitaria, CP 04510, México DF, México. E-mail: aps{at}fciencias.unam.mx
ABSTRACT
Pulmonary fibrosis, the final result of a large variety of interstitial lung diseases, is characterized by an aberrant remodeling of extracellular matrix (ECM) with a profound disturbance of the normal lung architecture. This remodeling includes the exaggerated accumulation of ECM components in the interstitial and alveolar spaces and the disruption of the basement membranes. It has long been accepted that matrix metalloproteases (MMPs) play an important role in the pathogenesis of pulmonary fibrosis, but the exact mechanisms are not well characterized. Several MMPs are strongly up-regulated in human and experimental lung fibrosis, highlighting the dynamic nature of scarring within the lung. MMPs are collectively capable of cleaving all components of the ECM and basement membranes, but importantly, they also process bioactive mediators such as growth factors, cytokines, chemokines, and cell-surface receptors. Moreover, they participate in the initiation of proteinase cascades that impact much broader substrates. Consequently, MMPs may play a central role in several interrelated processes observed in fibrosis such as ECM remodeling, basement-membrane breakdown, epithelial-cell apoptosis, cell migration, and angiogenesis.
Key Words: collagenase • gelatinase • matrilysin • matrix metalloproteinases • pulmonary fibrosis
This article has been cited by other articles:
|
|
 |
|
  A.-M. Pulichino, I-M. Wang, A. Caron, J. Mortimer, A. Auger, Y. Boie, J. A. Elias, A. Kartono, L. Xu, J. Menetski, et al. Identification of Transforming Growth Factor {beta}1-Driven Genetic Programs of Acute Lung Fibrosis Am. J. Respir. Cell Mol. Biol., September 1, 2008; 39(3): 324 - 336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Radisky and J. A. Przybylo Matrix Metalloproteinase-induced Fibrosis and Malignancy in Breast and Lung Proceedings of the ATS, April 15, 2008; 5(3): 316 - 322. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. L. Fattman, F. Gambelli, G. Hoyle, B. R. Pitt, and L. A. Ortiz Epithelial expression of TIMP-1 does not alter sensitivity to bleomycin-induced lung injury in C57BL/6 mice Am J Physiol Lung Cell Mol Physiol, March 1, 2008; 294(3): L572 - L581. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. C. Horowitz, D. S. Rogers, R. H. Simon, T. H. Sisson, and V. J. Thannickal Plasminogen Activation Induced Pericellular Fibronectin Proteolysis Promotes Fibroblast Apoptosis Am. J. Respir. Cell Mol. Biol., January 1, 2008; 38(1): 78 - 87. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. C. Willis and Z. Borok TGF-beta-induced EMT: mechanisms and implications for fibrotic lung disease Am J Physiol Lung Cell Mol Physiol, September 1, 2007; 293(3): L525 - L534. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Pierce, K. Carpenter, C. Jakubzick, S. L. Kunkel, K. R. Flaherty, F. J. Martinez, and C. M. Hogaboam Therapeutic Targeting of CC Ligand 21 or CC Chemokine Receptor 7 Abrogates Pulmonary Fibrosis Induced by the Adoptive Transfer of Human Pulmonary Fibroblasts to Immunodeficient Mice Am. J. Pathol., April 1, 2007; 170(4): 1152 - 1164. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-R. Kang, S. J. Cho, C. G. Lee, R. J. Homer, and J. A. Elias Transforming Growth Factor (TGF)-beta1 Stimulates Pulmonary Fibrosis and Inflammation via a Bax-dependent, Bid-activated Pathway That Involves Matrix Metalloproteinase-12 J. Biol. Chem., March 9, 2007; 282(10): 7723 - 7732. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |