Korea Identifies Key Role of ATF3 Gene in Idiopathic Pulmonary Fibrosis
- Seoyoung Kang
- May 1
- 1 min read
May 1, 2026
Seoyoung Kang
On the 28th of April, the Korea National Institute of Health Research identified a new function of the ATF3 gene that regulates immune adverse reactions during idiopathic pulmonary fibrosis progression.
Idiopathic pulmonary fibrosis is a chronic disease that causes shortness of breath due to the progression of unknown fibrosis in lung tissue. It usually occurs in smokers over the age of 50 and in the past, and the symptoms worsen gradually. There is no cure, but antifibrotic treatment can slow the progression.
Induced lung fibrosis in experimental animals lacking the ATF3 gene, lung capacity decreased by about 20 to 25% and lung elasticity increased compared to the normal group, resulting in a change in harder tissue. In addition, the inflammatory response increased significantly, resulting in abnormal changes in immune cell composition, such as a 10-fold increase in neutrophils and 6.5-fold increase in macrophages. Transcriptome analysis also revealed increased inflammation and fibrosis-related gene expression.
The researchers said, “We have identified a new molecular mechanism that simultaneously regulates the inflammatory response and tissue fibrosis of immune cells in the process of lung fibrosis. It is meaningful to confirm that the ATF3 gene plays a key role in suppressing excessive activation of the inflammatory response and alleviating the progression of lung fibrosis.”
These findings highlight the potential of ATF3 as a therapeutic target in treating pulmonary fibrosis. Further research is needed to explore its clinical applications in human patients.
