干细胞衍生的外泌体具有与其亲本干细胞相当的治疗效果，且不会造成免疫原性、致瘤性和伦理缺点。它们的治疗优势体现在治疗广泛的疾病中，并且它们的剂量多功能性体现在全身给药和局部给药。此外，各种信号级联的激活和调节为外泌体疗法所声称的疗效提供了基础。与其他关注干细胞源性外泌体疗法的上游方面（例如产量、分离、修饰）和下游方面（例如表型变化、组织反应、细胞行为）的相关评论不同，这篇独特的评论致力于关注各种受影响的领域信号通路。在对过去五年的相关文献进行仔细剖析后，我们提出了这篇全面的、最新的、针对疾病的、以路径为导向的综述。源自各种类型干细胞的外泌体可以调节主要信号传导途径（例如 PTEN/PI3K/Akt/mTOR、NF-κB、TGF-β、HIF-1α、Wnt、MAPK、JAK-STAT、Hippo 和 Notch 信号传导）级联）和次要途径，治疗骨科、神经外科、心胸外科、整形外科、普通外科和其他专业中遇到的许多疾病。我们在设计进一步的临床前研究和临床试验时，通过弥合信号通路和手术适应症之间的差距，为未来的外泌体研究提供了新颖的视角。© 2024。作者。

Stem cell-derived exosomes exert comparable therapeutic effects to those of their parental stem cells without causing immunogenic, tumorigenic, and ethical disadvantages. Their therapeutic advantages are manifested in the management of a broad spectrum of diseases, and their dosing versatility are exemplified by systemic administration and local delivery. Furthermore, the activation and regulation of various signaling cascades have provided foundation for the claimed curative effects of exosomal therapy. Unlike other relevant reviews focusing on the upstream aspects (e.g., yield, isolation, modification), and downstream aspects (e.g. phenotypic changes, tissue response, cellular behavior) of stem cell-derived exosome therapy, this unique review endeavors to focus on various affected signaling pathways. After meticulous dissection of relevant literature from the past five years, we present this comprehensive, up-to-date, disease-specific, and pathway-oriented review. Exosomes sourced from various types of stem cells can regulate major signaling pathways (e.g., the PTEN/PI3K/Akt/mTOR, NF-κB, TGF-β, HIF-1α, Wnt, MAPK, JAK-STAT, Hippo, and Notch signaling cascades) and minor pathways during the treatment of numerous diseases encountered in orthopedic surgery, neurosurgery, cardiothoracic surgery, plastic surgery, general surgery, and other specialties. We provide a novel perspective in future exosome research through bridging the gap between signaling pathways and surgical indications when designing further preclinical studies and clinical trials.© 2024. The Author(s).