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Published on: December 21, 2014

Matrix metalloproteinase-9 in lung remodeling

Jeffrey J Atkinson1, Robert M Senior

  • 1Pulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri 63110, USA.

American Journal of Respiratory Cell and Molecular Biology
|December 24, 2002
PubMed

Insights

Matrix metalloproteinase-9 (MMP-9) is elevated in lung diseases like asthma, IPF, and COPD. Its exact role in lung remodeling and disease progression requires further investigation for potential therapeutic targeting.

Area of Science:

  • Pulmonary Medicine
  • Biochemistry
  • Cell Biology

Background:

  • Matrix metalloproteinase-9 (MMP-9) is significantly upregulated in the lungs of patients with asthma, idiopathic pulmonary fibrosis (IPF), and chronic obstructive pulmonary disease (COPD) compared to healthy individuals.
  • While MMP-9 is produced by various lung cells, its specific contribution to lung remodeling versus its role in inflammatory and reparative processes remains unclear.
  • MMP-9 has diverse functions, including the degradation of structural proteins and antiproteases, and can modulate cellular activities through cytokine and growth factor regulation.

Purpose of the Study:

  • To review the current understanding of MMP-9's role in human asthma, IPF, and COPD.
  • To explore MMP-9's involvement in both human diseases and relevant animal models.
  • To highlight the importance of determining MMP-9's function for future therapeutic interventions.

Main Methods:

  • Literature review of studies investigating MMP-9 in human lung diseases and animal models.
  • Analysis of existing data on MMP-9 production by intrinsic lung cells and inflammatory cells.
  • Synthesis of information regarding MMP-9's enzymatic and regulatory functions in the lung microenvironment.

Main Results:

  • MMP-9 is abundant in several lung diseases, suggesting a significant role beyond its low levels in healthy lungs.
  • Multiple cell types contribute to MMP-9 production, indicating varied functions depending on the microenvironment.
  • MMP-9's dual capacity to degrade matrix components and regulate cellular signaling underscores its complex involvement in lung pathology.

Conclusions:

  • Further research is crucial to elucidate whether MMP-9 is a driver of lung remodeling or a component of the body's response to lung injury.
  • Understanding MMP-9's precise role is essential for the development of targeted therapies, as specific inhibitors are nearing clinical application.
  • This review consolidates current knowledge on MMP-9 in major human lung diseases, paving the way for future clinical translation.

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