胡荣贵 Ronggui Hu

胡荣贵教授长期致力于从解析蛋白质稳态网络与分子信号途径出发探讨重大疾病发生发展机制。近年来课题组的一部分逐步转向探索儿童自闭症谱系障碍等神经精神发育疾病的分子神经生物学基础。课题组建立了病人来源的诱导多能干细胞、类器官、小鼠、非人灵长类动物等疾病模型，应用离体脑片、光遗传和神经元成像、在体电生理技术等结合遗传学筛选、空间多组学，在分子、细胞、神经环路、行为学等深入探讨儿童自闭症谱系障碍(ASD)、中枢性性早熟(CPP)等儿童精神神经发育疾病发生发展的机制。课题组前期发现维甲酸代谢及信号通路异常导致多种亚型的儿童自闭症谱系障碍(ASD)，目前研究方向包括：儿童自闭症谱系障碍以及焦虑、抑郁等情绪行为异常的分子神经生物学基础、神经系统与外周器官交互及共病机制、疾病遗传与风险因素鉴定、发展靶点分子稳态的生物感应器、体内成像工具和疾病靶向干预新策略。

Professor Ronggui Hu has long been dedicated to exploring the mechanisms of major disease occurrence and development by analyzing protein homeostasis networks and molecular signaling pathways. In recent years, part of the research group has gradually shifted to exploring the molecular neurobiological basis of neurodevelopmental psychiatric disorders such as autism spectrum disorders in children. The group has established disease models including patient-derived induced pluripotent stem cells, organoids, mice, and non-human primates, and applied ex vivo brain slices, optogenetics and neuronal imaging, in vivo electrophysiology combined with genetic screening and spatial multi-omics to deeply investigate the mechanisms of neurodevelopmental psychiatric disorders such as autism spectrum disorders (ASD) and central precocious puberty (CPP) in children at molecular, cellular, neural circuit, and behavioral levels. The group previously discovered that abnormalities in retinoic acid metabolism and signaling pathways lead to multiple subtypes of autism spectrum disorders (ASD) in children. Current research directions include: molecular neurobiological basis of autism spectrum disorders and emotional behavioral abnormalities such as anxiety and depression in children, neural system and peripheral organ interactions and comorbidity mechanisms, disease genetics and risk factor identification, development of biosensors for target molecular homeostasis, in vivo imaging tools, and novel disease-targeted intervention strategies.

1. Hao, Z., et al., Hu R.*. Maternal exposure to triclosan constitutes a yet unrecognized risk factor for autism spectrum disorders. Cell Res 29, 866–869 (2019).
2. Xu X, et al, Hu R*. Excessive UBE3A dosage impairs retinoic acid signaling and synaptic plasticity in autism spectrum disorders. Cell Res. 2018