Honors & Awards

  • AHA Postdoctoral Fellowship, American Heart Association (2025/01-2026/12)
  • Excellent doctoral dissertations in Liaoning Province, Education Department of Liaoning Province (2024)
  • Outstanding Doctoral Graduate in Liaoning Province, Educational Department of Liaoning Province (2023)
  • National Fellowship for Doctoral Student, Ministry of Education, PRC (2022)
  • Excellent Graduate Student in Shenyang, Shenyang Bureau Of Education (2022)
  • "Xtalpi" Fellowship, XtalPi Inc. (2021)

Professional Education

  • Ph.D., Shenyang Pharmaceutical University, Medicinal Chemistry (2023)
  • Joint-training Master, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Medicinal Chemistry (2020)
  • B.S., Shenyang Pharmaceutical University, Pharmacy (2018)

Stanford Advisors

  • Han Zhu, Postdoctoral Faculty Sponsor

Contact

  • Academic
    yinsun@stanford.edu
    University - Scholar Department: Cardiovascular Institute Operations Position: Postdoctoral Scholar

Additional Info

Links

All Publications

  • Novel Therapeutic Approach Targeting CXCR3 to Treat Immunotherapy Myocarditis. Circulation research Huang, Y. V., Sun, Y., Chou, H., Wagner, N., Vitale, M. R., Bayer, A. L., Xu, B., Lee, D., Lin, Z., Branche, C., Waliany, S., Neal, J. W., Wakelee, H. A., Witteles, R. M., Nguyen, P. K., Graves, E. E., Berry, G. J., Alcaide, P., Wu, S. M., Zhu, H. 2025

    Abstract

    Immune checkpoint inhibitors (ICIs) are successful in treating many cancers but may cause immune-related adverse events. ICI-mediated myocarditis has a high fatality rate with severe cardiovascular consequences. Targeted therapies for ICI myocarditis are currently limited.We used a genetic mouse model of PD1 deletion (MRL/Pdcd1-/-) along with a novel drug-treated ICI myocarditis mouse model to recapitulate the disease phenotype. We performed single-cell RNA-sequencing, single-cell T-cell receptor sequencing, and cellular indexing of transcriptomes and epitopes on immune cells isolated from MRL and MRL/Pdcd1-/- mice at serial time points. We assessed the impact of macrophage deletion in MRL/Pdcd1-/- mice, then inhibited CXCR3 (C-X-C motif chemokine receptor 3) in ICI-treated mice to assess the therapeutic effect on myocarditis phenotype. Furthermore, we delineated the functional and mechanistic effects of CXCR3 blockade on T-cell and macrophage interactions. We then correlated the results in human single-cell multiomics data from blood and heart biopsy data from patients with ICI myocarditis.Single-cell multiomics demonstrated expansion of CXCL (C-X-C motif chemokine ligand) 9/10+CCR2+ macrophages and CXCR3hi (C-X-C motif chemokine receptor 3 high-expressing) CD8+ (cluster of differentiation) effector T lymphocytes in the hearts of MRL/Pdcd1-/- mice correlating with onset of myocarditis development. Both depletion of CXCL9/10+CCR2+ (C-C motif chemokine receptor) macrophages and CXCR3 blockade, respectively, led to decreased CXCR3hi CD8+ T-cell infiltration into the heart and significantly improved survival. Transwell migration assays demonstrated that the selective blockade of CXCR3 and its ligand, CXCL10, reduced CXCR3+CD8+ T-cell migration toward macrophages, implicating this interaction in T-cell cardiotropism toward cardiac macrophages. Furthermore, cardiomyocyte apoptosis was induced by CXCR3hi CD8+ T cells. Cardiac biopsies from patients with confirmed ICI myocarditis demonstrated infiltrating CXCR3+ T cells and CXCL9+/CXCL10+ macrophages. Both mouse cardiac immune cells and patient peripheral blood immune cells revealed expanded TCR s (T-cell receptors) correlating with CXCR3hi CD8+ T cells in ICI myocarditis samples.These findings bring forth the CXCR3-CXCL9/10 axis as an attractive therapeutic target for ICI myocarditis treatment, and more broadly as a druggable pathway in cardiac inflammation.

    View details for DOI 10.1161/CIRCRESAHA.124.325652

    View details for PubMedID 39931812

https://orcid.org/0009-0000-8793-3169