Mitochondrial reactive oxygen species regulate transforming growth factor-β signaling.

TGF-β signaling is required for normal tissue repair; however, excessive TGF-β signaling can lead to robust profibrotic gene expression in fibroblasts, resulting in tissue fibrosis. TGF-β binds to cell-surface receptors, resulting in the phosphorylation of the Smad family of transcription factors to initiate gene expression. TGF-β also initiates Smad-independent pathways, which augment gene expression.

Keratinocyte growth factor expression is suppressed in early acute lung injury/acute respiratory distress syndrome by smad and c-Abl pathways.

Objective: Keratinocyte growth factor (KGF) is expressed primarily by fibroblasts, is important for alveolar epithelial proliferation/function, and protects against lung injury in multiple animal models. We wished to determine whether acute lung injury/acute respiratory distress syndrome (ALI/ARDS) alveolar fluid induces KGF and fibroblast genes important for alveolar repair.

Design: A single-center cohort study enrolling patients between 2004 and 2006.

Bronchoalveolar lavage fluid from patients with acute lung injury/acute respiratory distress syndrome induces myofibroblast differentiation.

Objective: Myofibroblasts express alpha-smooth muscle actin (alphaSMA), are important in tissue repair, and are present in the early phase of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). We wished to determine whether bronchoalveolar lavage fluid (BALF) from ALI/ARDS patients can induce myofibroblast differentiation and if this induction is associated with outcome.

Design: A single-center cohort study enrolling patients between 2002 and 2005.