The 2025 International Symposium on TGF-β Signaling Networks in Physiology and Pathology was successfully held at Nanchang University from October 21–23, 2025. The symposium was hosted by the Cell Signal Transduction Branch of the Chinese Society for Cell Biology and organized by the Ministry of Education Key Laboratory of Molecular Targeted Drug Discovery and Innovative Center for Solid Tumors and the School of Basic Medical Sciences of Nanchang University. It was co-organized by the Life Sciences Institute of Zhejiang University, the Jiangxi Society for Cell Biology, the Jiangxi Society for Biochemistry and Molecular Biology, and several other institutions. Professor Chen Ye-Guang served as Symposium Chair, with Professor Yan Xiao-Hua as Secretary-General. Over 300 experts, scholars, and faculty and students from Nanchang University, including participants from China and abroad, attended the international symposium.

The opening ceremony was chaired by Conference Chairman Professor Chen Ye-Guang, President of Nanchang University and Academician of the Chinese Academy of Sciences. In his welcoming remarks, Professor Chen extended a warm welcome to all attendees, with special thanks to the international guests who had traveled long distances to join the event. He highlighted the critical roles of the TGF-β signaling pathway in embryonic development, tissue homeostasis, and the pathogenesis of a wide range of human diseases. He expressed his hope that the symposium would serve as a vibrant platform for presenting the latest research advances, fostering scientific innovation and international collaboration, and accelerating interdisciplinary and translational efforts in the field.

The symposium focused on the signal transduction and regulation mechanisms of TGF-β family cytokines and their physiological and pathological functions. Several internationally renowned scholars and domestic experts in TGF-β research participated and presented their work.

· Signal Transduction and Regulation Mechanisms:

o Professor Carl-Henrik Heldin (Uppsala University, Sweden, and Royal Swedish Academy of Sciences) gave a keynote speech systematically introducing TGF-β-induced non-SMAD signaling pathways, their molecular mechanisms, and their crucial roles in tumors.

o Professor Peter ten Dijke (Leiden University Medical Center, Netherlands, and Academia Europaea/Royal Netherlands Academy of Arts and Sciences) presented his finding that a mouse parasite regulates host response by secreting TGF-β mimics (TGMs).

o Professor Zhang Long (Zhejiang University/Nanchang University) reported on the role and mechanism of how mammalian cells sense L-lactate via alanyl-tRNA synthetase AARS1/2, and directly catalyze protein lactylation modification to regulate TGF-β signal transduction.

· Physiological Functions of TGF-β Family Proteins:

o Professor Xu Pengfei (Zhejiang University School of Medicine) used pluripotent stem cells, zebrafish, and mice as models to introduce the functions and mechanisms of Nodal and BMPs in early embryonic development and tissue/organ formation.

o Professor Wang Qiong (Shanghai Jiao Tong University School of Medicine) shared her research using multi-omics techniques to study the signal regulation network and epigenetic regulatory mechanisms of the TGF-β/Smad pathway during embryonic stem cell differentiation into mesoderm.

o Associate Professor Yu Yi (Life Sciences Institute, Zhejiang University) reported that Smad9 suppresses BMP/Smad1 signal-induced gene transcription by recruiting deacetylase HDAC1, thus impacting cardiac development.

· Disease Research:

o Professor Steven Dooley (Heidelberg University, Germany) shared his latest results on how TGF-β signaling regulates the onset and progression of chronic liver disease and liver cancer.

o Researcher Wang Cun (Shanghai Cancer Institute) used kinome and CRISPR screening to discover that DYRK1A kinase can directly phosphorylate and inhibit the activity of Smad3, thereby lifting the TGF-β-mediated transcriptional repression of the glutamine transporter SLC1A5. Inhibiting DYRK1A can enhance the sensitivity of liver cancer cells to OXPHOS inhibition.

o Professor Xi Qiaoran (School of Life Sciences, Tsinghua University) found that the histone H3.3K27M mutation promotes Diffuse Intrinsic Pontine Glioma (DIPG) by increasing the expression of BMP inhibitors, and also revealed the mechanism and function of the interaction between DIPG tumor cells and neural precursor cells.

o Professor Keiji Miyazawa (Yamanashi University, Japan) studied the molecular mechanism by which constitutively active SMAD3 mutants (S264T and S264F), found in patients with melorheostosis, stimulate the transcription of TGF-β target genes.

· Targeting Intervention and Translational Applications:

o Professor Andrew P. Hinck (University of Pittsburgh, USA) first systematically introduced the specificity mechanism of TGF-β ligand-receptor interaction from a structural biology perspective. He then reported an example of a protein-based inhibitor currently in cancer immunotherapy clinical trials that targets TGF-β signaling and intervenes in tumor development through a unique binding mode.

o Professor Seong-Jin Kim (Director of GILO Foundation Institute, South Korea, and Academician of the Korean Academy of Science and Technology) presented the clinical trial results of a new TGF-β Type I receptor kinase inhibitor (Vactosertib), which enhances anti-tumor efficacy when combined with various cancer treatments.

The symposium featured rich content and enthusiastic discussions. It advanced the understanding of the mechanisms and functions of the TGF-β family signaling network, and deliberated on the major scientific questions, future research directions, and the potential and pathways for translational application in the field. The successful convening of the conference provided a valuable opportunity for Nanchang University's faculty and students to interact closely with renowned domestic and international experts and scholars, and is beneficial for promoting the advancement of biomedical research at the university.