The study investigates the angiogenic properties of the human cathelicidin antimicrobial peptide LL-37/hCAP-18. LL-37 is expressed in various immune and epithelial cells and has been shown to have antimicrobial and immunomodulatory functions. The research demonstrates that LL-37 induces angiogenesis, the formation of new blood vessels, both in physiological and pathological contexts. In vitro and in vivo experiments, including the chorioallantoic membrane assay and a rabbit hind-limb ischemia model, show that LL-37 promotes neovascularization by directly activating endothelial cells. The angiogenic activity of LL-37 is mediated through its interaction with formyl peptide receptor-like 1 (FPRL1) on endothelial cells, leading to increased cell proliferation and the formation of vessel-like structures. Additionally, the study finds that mice lacking the murine homologue of LL-37, CRAMP, exhibit reduced wound revascularization, further supporting the role of LL-37 in angiogenesis. The findings highlight the multifunctional role of LL-37/hCAP-18 in linking innate immunity, inflammation, and angiogenesis, suggesting potential therapeutic applications in conditions requiring angiogenesis.The study investigates the angiogenic properties of the human cathelicidin antimicrobial peptide LL-37/hCAP-18. LL-37 is expressed in various immune and epithelial cells and has been shown to have antimicrobial and immunomodulatory functions. The research demonstrates that LL-37 induces angiogenesis, the formation of new blood vessels, both in physiological and pathological contexts. In vitro and in vivo experiments, including the chorioallantoic membrane assay and a rabbit hind-limb ischemia model, show that LL-37 promotes neovascularization by directly activating endothelial cells. The angiogenic activity of LL-37 is mediated through its interaction with formyl peptide receptor-like 1 (FPRL1) on endothelial cells, leading to increased cell proliferation and the formation of vessel-like structures. Additionally, the study finds that mice lacking the murine homologue of LL-37, CRAMP, exhibit reduced wound revascularization, further supporting the role of LL-37 in angiogenesis. The findings highlight the multifunctional role of LL-37/hCAP-18 in linking innate immunity, inflammation, and angiogenesis, suggesting potential therapeutic applications in conditions requiring angiogenesis.