FPR1 driven neutrophil-endothelial cell axis promotes inflammation resolution and angiogenesis in peripheral artery occlusive disease
FPR1 is a well-established mediator of host defense and a regulator of inflammation and tissue regeneration. However, the specific downstream signaling pathways through which FPR1 acts in limb ischemia to resolve inflammation and promote angiogenesis remain unexplored. To address this gap, we investigated the signaling pathways altered in the gastrocnemius muscle following hindlimb ischemia (HLI). We then performed gene-expression profiling using RNA-seq data from wild-type mice (sham, HLI, HLI + Cmpd17b) and Fpr1 knockout mice (sham, HLI).