棘球蚴病是世界范围内最严重、最危及生命的人畜共患寄生虫病之一，由细粒棘球蚴 (E. capsulosus) 和多房棘球绦虫 (E. multilularis) 的幼虫引起。临床上正在应用多种药物来治疗人畜共患疾病；然而，它们的治疗效果仍然是一个巨大的挑战，特别是在阿苯达唑作为首选药物的情况下。受体酪氨酸激酶 (RTK) 信号传导控制人类和哺乳动物的正常细胞增殖、分化和代谢，人类和哺乳动物是细粒棘球绦虫和多房棘球绦虫的中间宿主。 RTK 信号传导的破坏可能导致各种形式的致癌作用，并加剧某些形式的寄生虫病的进展。因此，针对酪氨酸激酶抑制剂（TKI）用于治疗癌症和寄生虫感染进行了大量研究，其中一些 TKI 已被批准用于临床治疗癌症。值得注意的是，RTK 信号传导已在寄生虫细粒艾美耳球虫和多房艾美耳球虫中得到鉴定。然而，棘球蚴-宿主相互通讯中RTK信号响应的机制尚不完全清楚。因此，了解棘球绦虫与宿主相互通讯中的 RTK 信号反应以及 RTK 信号的潜在影响对于确定包虫病的新药物靶点至关重要。本综述表明，在细粒艾美耳球虫或多房艾美耳球虫感染后，宿主中的 RTK 信号传导过度激活，并且可以进一步促进后绦虫在体外的发育。此外，一些 TKI 通过下调 RTK 信号分子，在体外和/或体内对细粒艾美耳球虫或多房艾美耳球虫产生强烈的寄生虫抑制作用。总结的结果表明，RTK 信号传导可能是一个有前途的药物靶点，并且 TKI 可能是值得进一步研究的潜在抗棘球绦虫药物。

Echinococcosis, one of the most serious and life-threatening parasitic forms of zoonosis worldwide, is caused by the larvae of Echinococcus granulosus (E. granulosus) and Echinococcus multilocularis (E. multilocularis). Various drugs are being applied clinically to treat zoonosis; however, their therapeutic efficacy remains a great challenge, especially with albendazole as the preferred drug of choice. Receptor tyrosine kinase (RTK) signaling controls normal cellular proliferation, differentiation, and metabolism in humans and mammals, which are intermediate hosts of E. granulosus and E. multilocularis. Disruption of RTK signaling can cause various forms of carcinogenesis and exacerbate the progression of certain forms of parasitic disease. As a result, a significant number of studies on tyrosine kinase inhibitors (TKIs) have been conducted for the treatment of cancer and parasitic infection, with some TKIs already approved for clinical use for cancer. Notably, RTK signaling has been identified in the parasites E. granulosus and E. multilocularis; however, the mechanisms of RTK signaling response in Echinococcus-host intercommunication are not fully understood. Thus, understanding the RTK signaling response in Echinococcus-host intercommunication and the potential effect of RTK signaling is crucial for identifying new drug targets for echinococcosis. The present review illustrates that RTK signaling in the host is over-activated following infection by E. granulosus or E. multilocularis and can further facilitate the development of metacestodes in vitro. In addition, some TKIs exert strong parasitostatic effects on E. granulosus or E. multilocularis, both in vitro and/or in vivo, through downregulation of RTK signaling molecules. The summarized findings suggest that RTK signaling may be a promising drug target and that TKIs could be potential anti-Echinococcus drugs warranting further research.