Our HCF proteomic analysis demonstrated that expression of the cytoskeleton protein Msn was greater in Ang II-stimulated HCFs, consistent with its critical role in pulmonary oedema caused by heart failure.36 Interestingly, our data demonstrated that Cmpd17b reduces Msn expression in human hypertensive cardiac fibroblasts, suggesting that FPR agonism may lead to a decrease in Msn-mediated re-arrangements of cytoskeleton. This evidence concerns the gene AGT and pulmonary edema.