IGF-1 inhibits inflammation and accelerates angiogenesis via Ras/PI3K/IKK/NF-κB signaling pathways to promote wound healing

• Published in: European journal of pharmaceutical sciences 2024-09, Vol.200, p.106847, Article 106847
• Main Authors: Zhang, Xin, Hu, Fei, Li, Jie, Chen, Lin, Mao, Yu-fei, Li, Qiu-bo, Nie, Chen-yao, Lin, Cai, Xiao, Jian
• Format: Article
• Language: English
• Subjects: Angiogenesis; IGF-1; Inflammation; Signaling pathways; Wound healing
• ISSN: 0928-0987; 1879-0720; 1879-0720
• DOI: 10.1016/j.ejps.2024.106847

Exogenous insulin-like growth factor-1 (IGF-1) has been reported to promote wound healing through regulation of vascular endothelial cells (VECs). Despite the existing studies of IGF-1 on VEC and its role in angiogenesis, the mechanisms regarding anti-inflammatory and angiogenetic effects of IGF-1 remain unclear. In this study, we investigated the wound-healing process and the related signaling pathway of IGF-1 using an inflammation model induced by IFN-γ. The results demonstrated that IGF-1 can increase cell proliferation, suppress inflammation in VECs, and promote angiogenesis. In vivo studies further confirmed that IGF-1 can reduce inflammation, enhance vascular regeneration, and improve re-epithelialization and collagen deposition in acute wounds. Importantly, the Ras/PI3K/IKK/NF-κB signaling pathways was identified as the mechanisms through which IGF-1 exerts its anti-inflammatory and pro-angiogenic effects. These findings contribute to the understanding of IGF-1′s role in wound healing and may have implications for the development of new wound treatment approaches. [Display omitted]