Sonic hedgehog (SHh)信号通路是一个至关重要的工作网络，可以在多细胞胚胎生长和形态建立等发育过程中调节关键事件。SHh通路调控的紊乱可能导致严重后果，包括先天性残疾、干细胞更新、组织再生以及癌症/肿瘤生长等。当SHh结合到Patch (Ptc)-介导的Smoothened (Smo) (Ptc-smo)受体复合物上时，SHh信号的激活就开始了，随后启动下游信号传导。本综述研究了SHh通路药理调控对通过经典和非经典途径影响血管生成的情况。经典途径血管生成包括激活血管生成细胞因子，如成纤维细胞生长因子(FGF)、血管内皮生长因子(VEGF)、胎盘生长因子(PGF)、肝细胞生长因子(HGF)、血小板源性生长因子(PDGF)、基质细胞源性因子1α、转化生长因子-β1(TGF-β1)和血管生成素(Ang-1和Ang-2)，从而促进血管生成过程。非经典途径包括间接激活特定通路，如iNOS/Netrin-1/PKC、RhoA/Rock、ERK/MAPK、PI3K/Akt、Wnt/β-连环蛋白、Notch信号通路等。本综述将更好地阐明SHh在介导血管生成中的机制，有助于抑制特定癌症和肿瘤生长。版权所有 © 2023. Elsevier Inc.出版。

The Sonic hedgehog (SHh) signaling pathway is an imperative operating network that helps in regulates the critical events during the development processes like multicellular embryo growth and patterning. Disruptions in SHh pathway regulation can have severe consequences, including congenital disabilities, stem cell renewal, tissue regeneration, and cancer/tumor growth. Activation of the SHh signal occurs when SHh binds to the receptor complex of Patch (Ptc)-mediated Smoothened (Smo) (Ptc-smo), initiating downstream signaling. This review explores how pharmacological modulation of the SHh pathway affects angiogenesis through canonical and non-canonical pathways. The canonical pathway for angiogenesis involves the activation of angiogenic cytokines such as fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), placental growth factor (PGF), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF), stromal cell-derived factor 1α, transforming growth factor-β1 (TGF-β1), and angiopoietins (Ang-1 and Ang-2), which facilitate the process of angiogenesis. The Non-canonical pathway includes indirect activation of certain pathways like iNOS/Netrin-1/PKC, RhoA/Rock, ERK/MAPK, PI3K/Akt, Wnt/β-catenin, Notch signaling pathway, and so on. This review will provide a better grasp of the mechanistic approach of SHh in mediating angiogenesis, which can aid in the suppression of certain cancer and tumor growths.Copyright © 2023. Published by Elsevier Inc.