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1
Fibrinogen-like protein 2 (FGL2) is implicated in airway smooth muscle cell (ASMC) dysfunction and modulates inflammatory responses.
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2
PDGF-BB stimulation significantly increases FGL2 expression in ASMCs, enhancing proliferation, migration, and inflammation.
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3
Silencing FGL2 reduces PI3K/Akt pathway activation, leading to decreased ASMC proliferation, migration, and inflammatory cytokine production.
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4
FGL2 knockdown also inhibits glycolytic reprogramming in ASMCs, affecting glucose consumption and lactate production.
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5
These findings suggest FGL2 as a potential therapeutic target for chronic airway diseases by limiting airway remodeling.