Objective:

To investigate the role of FGL2 in PDGF-BB-induced pathological responses, specifically proliferation, migration, and inflammation, in airway smooth muscle cells (ASMCs) and explore the underlying signaling mechanisms.

Key Findings:

• PDGF-BB stimulation increased FGL2 expression in ASMCs.
• Silencing FGL2 attenuated PDGF-BB-induced PI3K/Akt activation.
• FGL2 knockdown suppressed ASMC proliferation, migration, and ECM protein expression.
• FGL2 depletion reduced proinflammatory cytokines and oxidative stress markers.
• Glycolytic reprogramming induced by PDGF-BB was inhibited by FGL2 knockdown.

Interpretation:

FGL2 plays a critical role in PDGF-BB-induced ASMC dysfunction by modulating the PI3K/Akt signaling pathway, which affects key processes such as proliferation, inflammation, oxidative stress, and metabolism.

Limitations:

• The study is preliminary and requires further investigation to validate findings in vivo.
• The in vitro nature of the study may limit the applicability of findings to in vivo conditions, necessitating caution in extrapolating results.

Conclusion:

FGL2 could represent a potential therapeutic target for limiting airway remodeling in chronic airway diseases.