Skip to main content
Fig. 1 | Lipids in Health and Disease

Fig. 1

From: The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases

Fig. 1

The mechanism of PF. â‘  Excessive apoptosis of endothelial and epithelial cells leads to lung injury and releases various pro-inflammatory and profibrotic factors. Injured EC and alveolar epithelial cells also undergo senescence, inducing an SASP phenotype, which further enhances the pro-inflammatory and profibrotic effects. â‘¡ The apoptosis-resistant endothelial and epithelial cells undergo an activated process to obtain fibroblast-like properties. â‘¢ The polarisation of macrophages confers AM and IM cells to differentiate into activated macrophages, which produce abundant pro-inflammatory and profibrotic factors and further promote PF. â‘£ Over-proliferation and hyperactivation of fibroblast lead to ECM deposition and fibrosis formation

Back to article page

Lipids in Health and Disease

ISSN: 1476-511X