S100A4 and chronic asthma: Furthermore, the airway remodeling in the chronic asthma model was confirmed to be attenuated by inhibition of soluble epoxide hydrolase, dapagliflozin and ZDHXB-101 (3’,5-Diallyl-2, 4’-dihydroxy-[1,1’-biphen-yl]-3,5’-dicarbaldehyde), and the expression of remodeling-related molecular markers reduced, including S100A4.[42–44] An in-depth study showed that the synthesis and secretion of S100A4 in airway smooth muscle tissues could be stimulated by inflammatory mediators and that extracellular S100A4 acted via RAGE to mediate airway smooth muscle inflammation.[45]