scholarly journals Matrix metalloproteinase‐2, ‐7, and ‐9 activities in dogs with idiopathic pulmonary fibrosis compared to healthy dogs and dogs with other respiratory diseases

2020 ◽  
Author(s):  
Merita Määttä ◽  
Henna P. Laurila ◽  
Saila Holopainen ◽  
Kaisa Aaltonen ◽  
Liisa Lilja‐Maula ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Matrix Metalloproteinase ◽  
Respiratory Diseases ◽  
Matrix Metalloproteinase 2 ◽  
Healthy Dogs

scholarly journals Differential diagnosis of idiopathic pulmonary fibrosis

2020 ◽  
Vol 92 (3) ◽  
pp. 102-108
Author(s):  
E. I. Shmelev ◽  
A. E. Ergeshov ◽  
V. Ya. Gergert
Keyword(s):  
Differential Diagnosis ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Diseases ◽  
Respiratory Diseases ◽  
Clinical Signs ◽  
Interstitial Lung Diseases ◽  
Antifibrotic Therapy ◽  
Inflammatory Drugs ◽  
Diffuse Lung

The review is devoted to the urgent problem of modern pulmonology: the differential diagnosis of idiopathic pulmonary fibrosis (ILF). ILF occupies a special place among many interstitial lung diseases for a number of reasons: 1) it is a deadly disease; 2) early diagnosis and adequate antifibrotic therapy significantly extend the life expectancy of patients; 3) anti-inflammatory drugs (corticosteroids) and cytostatics with ILF that are widely used in other forms of interstitial lung diseases are ineffective and accelerate the progression of the process; 4) the commonality of the main clinical signs (increasing respiratory failure) of various interstitial lung diseases. The list of respiratory diseases with which ILF should be differentiated is huge, and if with diffuse lung lesions of a known nature (disseminated pulmonary tuberculosis, pneumoconiosis, etc.) with a certain experience/qualification, the diagnosis is relatively simple, then the isolation of ILF from the group of idiopathic interstitial pneumonias always represents certain difficulties. The main methods used in the diagnosis of ILF are summarized taking into account current international and national recommendations.

Matrix Metalloproteinase in Idiopathic Pulmonary Fibrosis

2001 ◽  
Vol 51 (4) ◽  
pp. 303 ◽  
Author(s):  
Joohun Park ◽  
Tae Sun Shim ◽  
Chae Man Lim ◽  
Younsuck Koh ◽  
Sang Do Lee ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Matrix Metalloproteinase

scholarly journals Matrix metalloproteinase-10: a novel biomarker for idiopathic pulmonary fibrosis

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Akihiko Sokai ◽  
Tomohiro Handa ◽  
Kiminobu Tanizawa ◽  
Toru Oga ◽  
Kazuko Uno ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Matrix Metalloproteinase

scholarly journals Allele-specific transactivation of matrix metalloproteinase 7 by FOXA2 and correlation with plasma levels in idiopathic pulmonary fibrosis

2012 ◽  
Vol 302 (8) ◽  
pp. L746-L754 ◽  
Author(s):  
Thomas J. Richards ◽  
Chunghyun Park ◽  
Yiliang Chen ◽  
Kevin F. Gibson ◽  
Y. Peter Di ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Matrix Metalloproteinase ◽  
Plasma Levels ◽  
Complex Disease ◽  
Proper Function ◽  
Promoter Polymorphisms ◽  
Matrix Metalloproteinase 7 ◽  
Increased Sensitivity

Idiopathic pulmonary fibrosis (IPF) is a complex disease with poorly understood etiology. Previously, we reported upregulation of matrix metalloproteinase 7 (MMP7) in both lung and peripheral blood of IPF patients. Here we report evidence for genetic correlation of plasma levels and promoter polymorphisms (rs11568818 and rs11568819) of MMP7 in a well-characterized IPF cohort. Both the AA genotype of rs11568818 and the CT genotype of rs11568819 were found to be significantly associated with higher MMP7 plasma levels. These associations were observed only in IPF patients and not in healthy controls. The G-to-A transition of rs11568818 resulted in a novel binding site for the forkhead box A2 (FOXA2) transcription factor, a key regulator of embryonic lung development and proper function of the mature lung. In vitro, this transition led to increased sensitivity of the MMP7 promoter to FOXA2. In IPF lungs, FOXA2 was localized in the nucleus of epithelial cells that expressed MMP7 in the cytoplasm. These results suggest that increased sensitivity of the polymorphic MMP7 promoter to FOXA2 provides one of the genetic bases for the upregulation of MMP7 in IPF.

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