Please note that eDoc will be permanently shut down in the first quarter of 2021!      Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Quick Search
My eDoc
Session History
Support Wiki
Direct access to
document ID:

          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook_2014     Display Documents

ID: 682195.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook_2014
Mast cell chymase: an indispensable instrument in the pathological symphony of idiopathic pulmonary fibrosis?
Authors:Kosanovic, D.; Dahal, B. K.; Wygrecka, M.; Reiss, I.; Gunther, A.; Ghofrani, H. A.; Weissmann, N.; Grimminger, F.; Seeger, W.; Schermuly, R. T.; Banat, G. A.
Date of Publication (YYYY-MM-DD):2013-06
Journal Abbrev.:Histol Histopathol
Issue / Number:6
Start Page:691
End Page:699
Audience:Not Specified
Abstract / Description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal lung disease with no known etiology and treatment options. The hallmarks of the histopathology, which is characteristic of usual interstitial pneumonia (UIP) pattern, include interstitial fibrosis, honeycomb changes and fibroblast foci that develop owing to fibroblast proliferation and excessive matrix deposition. Although the complete pathomechanism is not yet understood, several molecular culprits, including transforming growth factor (TGF)-beta, Angiotensin (Ang) II, endothelin (ET)-1, matrix metalloproteinases (MMPs) and cytokines have been identified. IPF is increasingly believed to be an epithelial-driven disease; however, the literature does support an implication of altered immune response and inflammatory processes in the onset or progression of the disease. Mast cells (MCs) are multifunctional tissue resident cells involved in the inflammatory and immune response. An increasing body of evidence suggests a role of MCs and their mediator chymase in the pathology of IPF. With regard to the underlying mechanisms, it is conceivable that MC chymase may function via activation or processing of factors such as proteases, cytokines and growth factors. In this review, we will discuss how MC chymase is linked to and can potentially contribute to the development of IPF. Moreover, the findings from animal model studies will be discussed to highlight the chymase inhibitors as a promising strategy for the treatment of pulmonary fibrosis.
Free Keywords:Animals; Biological Markers/metabolism; Chymases/*metabolism; Disease Models, Animal; Humans; Idiopathic Pulmonary Fibrosis/enzymology/immunology/*pathology; Lung/immunology/metabolism/pathology; Mast Cells/*enzymology/immunology; Mice
External Publication Status:published
Document Type:Article
Communicated by:Svea Hümmer
Affiliations:MPI für physiologische und klinische Forschung
Identifiers:ISSN:1699-5848 (Electronic) 0213-3911 (Linking)
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.