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Role of gelatinases MMP-2 and MMP-9 in tissue remodeling following acute lung injury.
TLDR
This review details the knowledge of the involvement of MMPs, namely M MP-2 and MMP-9, in acute lung injury and acute respiratory distress syndrome.
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Role of matrix metalloproteinases in the development of airway inflammation and remodeling.
TLDR
The correlation of the differences in hydroxyproline levels in the lungs of bleomycin-treated mice strongly suggests that a reduced molar pro-MMP-9/TIMP-1 ratio in bronchoalveolar lavage fluid is associated with collagen deposition, beginning as early as the inflammatory events at day 1 afterBleomycin administration.
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Involvement of gelatinases (MMP-2 and MMP-9) in the development of airway inflammation and pulmonary fibrosis
TLDR
The excessive airway remodeling as a result of an imbalance in the equilibrium of the normal processes of synthesis and degradation of extracellular matrix components could argue in favor of antiprotease treatments.
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Inhibition of bleomycin‐induced pulmonary fibrosis in mice by the matrix metalloproteinase inhibitor batimastat
TLDR
Results suggest that administration of the MMP inhibitor batimastat is useful in preventing experimental pulmonary fibrosis induced by bleomycin and raises the possibility of a therapeutic approach to human pulmonary fibrotic disease.
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Macrophage metalloelastase (MMP-12) as a target for inflammatory respiratory diseases.
TLDR
MMP-12 plays a predominant role in the inflammatory process induced by cigarette smoke, and therefore is potentially an important therapeutic target for the treatment of COPD.
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Involvement of matrix metalloproteinases (MMPs) and inflammasome pathway in molecular mechanisms of fibrosis
TLDR
Using the carbon tetrachloride preclinical model of liver fibrosis in mice, a significant increase in collagen deposition with increased expression and release of tissue inhibitors of metalloproteinase (TIMP)-1 suggests an early altered regulation of matrix turnover involved in the development of fibrosis.
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Effects of cannabinoid receptor ligands on LPS-induced pulmonary inflammation in mice.
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Characterization of the MMP/TIMP Imbalance and Collagen Production Induced by IL-1β or TNF-α Release from Human Hepatic Stellate Cells
TLDR
The results suggest that pro-inflammatory mediators exert complex effects in HSCs via an MMP/TIMP imbalance, and targeting IL-1 signaling may be a potentially valuable therapeutic strategy in chronic liver diseases.
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Macrophage elastase (MMP-12): a pro-inflammatory mediator?
TLDR
The instillation of a recombinant form of human MMP-12 in mouse airways induced a severe inflammatory cell recruitment characterized by an early accumulation of neutrophils correlated with an increase in proinflammatory cytokines and in gelatinases and indicated that the model could mimic some of the inflammatory features observed in COPD patients and could be used for the pharmacological evaluation of new anti-inflammatory treatment.
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Cigarette Smoke-Induced Pulmonary Inflammation Is TLR4/MyD88 and IL-1R1/MyD88 Signaling Dependent1
TLDR
Airway inflammation is shown to be dependent on Toll-like receptor 4 and IL-1R1 signaling, which is crucial for cigarette smoke induced inflammation leading to chronic obstructive pulmonary disease with emphysema.
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