AIMS: We previously reported that tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-
SDKP) inhibited pulmonary inflammation and fibrosis in SiO2-induced silicosis. This study …

Damage to alveolar epithelial cells (AECs) caused by long-term inhalation of large amounts
of silica dust plays a significant role in the pathology of silicosis. The present study was …

Silicosis is the most serious occupational disease in China. The objective of this study was
to screen various proteins related to mechanisms of the pathogenesis of silicosis underlying …

New Findings What is the central question of this study? What are the effects of the
antifibrotic peptide acetyl‐seryl‐aspartyl‐lysyl‐proline (Ac‐SDKP) on the angiotensin …

The epithelial–mesenchymal transition (EMT) is a critical stage during the development of
silicosis fibrosis. In the current study, we hypothesized that the anti-fibrotic tetrapeptide, N …

Background Myofibroblast differentiation, characterized by α-smooth muscle actin (α-SMA)
expression, is a key process in organ fibrosis, and is induced by TGF-β. Here we examined …

Silicosis is a systemic disease characterized by diffuse fibrosis of the lung tissue caused by
long-term inhalation of large amounts of free silica (SiO 2) dust. The pathogenesis of …

Crystalline silica (SiO 2) particles have very strong toxicity to the lungs, and silicosis is an
excessive pulmonary interstitial remodeling disease that follows persistent SiO 2 injury. We …

Inhalation of crystalline silica particles leads to pulmonary fibrosis, eventually resulting in
respiratory failure and death. There are few effective drugs that can delay the progression of …

Silicosis is a refractory disease. Previous studies indicate that damaged alveolar epithelial
cells act as a driver in pulmonary fibrosis. Our results show that epithelial cells that acquire …