Regulation of transforming growth factor-β1-driven lung fibrosis by galectin-3.

ABSTRACT:

Rationale

Idiopathic pulmonary fibrosis (IPF) is a chronic dysregulated response to alveolar epithelial injury with differentiation of epithelial cells and fibroblasts into matrix-secreting myofibroblasts resulting in lung scaring. The prognosis is poor and there are no effective therapies or reliable biomarkers. Galectin-3 is a β-galactoside binding lectin that is highly expressed in fibrotic tissue of diverse etiologies.

Objectives

To examine the role of galectin-3 in pulmonary fibrosis.

Methods

We used genetic deletion and pharmacologic inhibition in well-characterized murine models of lung fibrosis. Further mechanistic studies were performed in vitro and on samples from patients with IPF.

Measurements and main results

Transforming growth factor (TGF)-β and

SUBMITTER: Mackinnon AC 

PROVIDER: S-EPMC3410728 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature