转化生长因子-β（TGF-β）超家族成员协调广泛的生物过程。通过Sma和Mad（Smad）相关依赖或非经典途径，TGF-β成员参与许多疾病的发生和发展，如癌症、纤维化、自身免疫性疾病、心血管疾病和脑疾病。糖基化是蛋白质或脂质最常见的一种翻译后修饰形式之一。异常蛋白质糖基化可能导致蛋白质功能失调和生物过程紊乱，从而引发严重疾病。以往，研究人员通常对TGF-β信号在特定疾病或生物过程中的作用进行全面系统的概述。近年来，越来越多的证据表明糖基化修饰与TGF-β信号通路相关，我们不能再忽略糖基化在TGF-β信号通路中的作用而不加以调查。在本综述中，我们概述了目前涉及TGF-β及其受体内的糖基化的研究进展，以及糖基化与TGF-β亚家族信号之间的相互作用效应，得出了糖基化与TGF-β信号之间存在复杂的相互调节关系，并希望呈现出隐藏在TGF-β信号通路中的糖基化调控模式。版权所有 © 2023 Elsevier B.V. 发布。

Transforming growth factor-beta (TGF-β) superfamily members orchestrate a wide breadth of biological processes. Through Sma and Mad (Smad)-related dependent or noncanonical pathways, TGF-β members involve in the occurrence and development of many diseases such as cancers, fibrosis, autoimmune diseases, cardiovascular diseases and brain diseases. Glycosylation is one kind of the most common posttranslational modifications on proteins or lipids. Abnormal protein glycosylation can lead to protein malfunction and biological process disorder, thereby causing serious diseases. Previously, researchers commonly make comprehensive systematic overviews on the roles of TGF-β signaling in a specific disease or biological process. In recent years, more and more evidences associate glycosylation modification with TGF-β signaling pathway, and we can no longer disengage and ignore the roles of glycosylation from TGF-β signaling to make investigation. In this review, we provide an overview of current findings involved in glycosylation within TGF-βs and theirs receptors, and the interaction effects between glycosylation and TGF-β subfamily signaling, concluding that there is an intricate mutual regulation between glycosylation and TGF-β signaling, hoping to present the glycosylation regulatory patterns that concealed in TGF-βs signaling pathways.Copyright © 2023. Published by Elsevier B.V.