Tongbin Wu, Ph.D.

Heart is one of the first organs developed in our body. In the embryonic heart, there is a meshwork of myocardial protrusions called trabeculae that extend from the ventricular wall into the ventricular lumen in the developing heart. As the heart matures from late embryonic stages through perinatal development, these trabecular structures undergo a critical process known as compaction. This process results in the disappearance of trabeculae and the thickening of the ventricular wall. The failure of proper compaction can lead to a heart disease known as left ventricular noncompaction (LVNC), which is the third most prevalent heart disease in the pediatric population and carries a significant risk of heart arrhythmias, thromboembolic events, and left ventricular dysfunction.

Our laboratory is dedicated to the investigation of transcription factors and post-transcriptional regulators that mutated or dysregulated in LVNC. Leveraging advanced techniques in mouse genetics and cutting-edge molecular biology and genomics tools, our research aims to unravel the intricate transcriptional and post-transcriptional networks involved in compaction and other critical processes in heart development. Our goal is to gain a deeper understanding of these networks, paving the way for the identification of novel therapeutic targets and the development of more effective treatments not only for LVNC but also for other heart diseases.


Tongbin Wu, Ph.D.
Assistant professor of biomedical research and translational medicine

Email –

Wu completed his Ph.D. in biochemistry and molecular biology at Wuhan University, Wuhan, China, and his postdoctoral training in molecular cardiology at the University of California San Diego (UCSD), San Diego, California. While at UCSD, Wu’s work was published in highly regarded scientific journals including, Circulation, PNAS, Circulation Research, PLOS Genetics and Nature Structure and Molecular Biology.



You can follow Tongbin on X @tongbinwu

Postdoctoral Fellows

- Zizhen Liu, Ph.D.

  1. Zhou, X, Fang, X, Ithychanda, SS, Wu, T, Gu, Y, Chen, C et al.. Interaction of Filamin C With Actin Is Essential for Cardiac Development and Function. Circ Res. 2023;133 (5):400-411. doi: 10.1161/CIRCRESAHA.123.322750. PubMed PMID:37492967 PubMed Central PMC10529502.
  2. Wu, T, Xu, Y, Zhang, L, Liang, Z, Zhou, X, Evans, SM et al.. Filamin C is Essential for mammalian myocardial integrity. PLoS Genet. 2023;19 (1):e1010630. doi: 10.1371/journal.pgen.1010630. PubMed PMID:36706168 PubMed Central PMC9907827.
  3. Bogomolovas, J, Zhang, Z, Wu, T, Chen, J. Automated quantification and statistical assessment of proliferating cardiomyocyte rates in embryonic hearts. Am J Physiol Heart Circ Physiol. 2023;324 (3):H288-H292. doi: 10.1152/ajpheart.00483.2022. PubMed PMID:36563012 PubMed Central PMC9886340.
  4. Wu, T, Liang, Z, Zhang, Z, Liu, C, Zhang, L, Gu, Y et al.. PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle. Circulation. 2022;145 (8):586-602. doi: 10.1161/CIRCULATIONAHA.121.056666. PubMed PMID:34915728 PubMed Central PMC8860879.
  5. Wu, T, Chen, J. p38 MAPK reins in right ventricular growth. J Clin Invest. 2020;130 (10):5109-5111. doi: 10.1172/JCI140793. PubMed PMID:32865520 PubMed Central PMC7524502.
  6. Liu, C, Spinozzi, S, Feng, W, Chen, Z, Zhang, L, Zhu, S et al.. Homozygous G650del nexilin variant causes cardiomyopathy in mice. JCI Insight. 2020;5 (16):. doi: 10.1172/jci.insight.138780. PubMed PMID:32814711 PubMed Central PMC7455123.
  7. Mu, Y, Yu, H, Wu, T, Zhang, J, Evans, SM, Chen, J et al.. O-linked β-N-acetylglucosamine transferase plays an essential role in heart development through regulating angiopoietin-1. PLoS Genet. 2020;16 (4):e1008730. doi: 10.1371/journal.pgen.1008730. PubMed PMID:32251422 PubMed Central PMC7182263.
  8. Liu, C, Spinozzi, S, Chen, JY, Fang, X, Feng, W, Perkins, G et al.. Nexilin Is a New Component of Junctional Membrane Complexes Required for Cardiac T-Tubule Formation. Circulation. 2019;140 (1):55-66. doi: 10.1161/CIRCULATIONAHA.119.039751. PubMed PMID:30982350 PubMed Central PMC6889818.
  9. Wu, T, Mu, Y, Bogomolovas, J, Fang, X, Veevers, J, Nowak, RB et al.. HSPB7 is indispensable for heart development by modulating actin filament assembly. Proc Natl Acad Sci U S A. 2017;114 (45):11956-11961. doi: 10.1073/pnas.1713763114. PubMed PMID:29078393 PubMed Central PMC5692592.
  10. Fang, X, Bogomolovas, J, Wu, T, Zhang, W, Liu, C, Veevers, J et al.. Loss-of-function mutations in co-chaperone BAG3 destabilize small HSPs and cause cardiomyopathy. J Clin Invest. 2017;127 (8):3189-3200. doi: 10.1172/JCI94310. PubMed PMID:28737513 PubMed Central PMC5531406.
  11. Fang, X, Stroud, MJ, Ouyang, K, Fang, L, Zhang, J, Dalton, ND et al.. Adipocyte-specific loss of PPARγ attenuates cardiac hypertrophy. JCI Insight. 2016;1 (16):e89908. doi: 10.1172/jci.insight.89908. PubMed PMID:27734035 PubMed Central PMC5053146.
  12. Shimoda, Y, Matsuo, K, Kitamura, Y, Ono, K, Ueyama, T, Matoba, S et al.. Diabetes-Related Ankyrin Repeat Protein (DARP/Ankrd23) Modifies Glucose Homeostasis by Modulating AMPK Activity in Skeletal Muscle. PLoS One. 2015;10 (9):e0138624. doi: 10.1371/journal.pone.0138624. PubMed PMID:26398569 PubMed Central PMC4580461.
  13. Wu, T, Fu, XD. Genomic functions of U2AF in constitutive and regulated splicing. RNA Biol. 2015;12 (5):479-85. doi: 10.1080/15476286.2015.1020272. PubMed PMID:25901584 PubMed Central PMC4615725.
  14. Shao, C, Yang, B, Wu, T, Huang, J, Tang, P, Zhou, Y et al.. Mechanisms for U2AF to define 3' splice sites and regulate alternative splicing in the human genome. Nat Struct Mol Biol. 2014;21 (11):997-1005. doi: 10.1038/nsmb.2906. PubMed PMID:25326705 PubMed Central PMC4429597.
  15. Domenighetti, AA, Chu, PH, Wu, T, Sheikh, F, Gokhin, DS, Guo, LT et al.. Loss of FHL1 induces an age-dependent skeletal muscle myopathy associated with myofibrillar and intermyofibrillar disorganization in mice. Hum Mol Genet. 2014;23 (1):209-25. doi: 10.1093/hmg/ddt412. PubMed PMID:23975679 PubMed Central PMC3916749.
  16. Xue, Y, Zhou, Y, Wu, T, Zhu, T, Ji, X, Kwon, YS et al.. Genome-wide analysis of PTB-RNA interactions reveals a strategy used by the general splicing repressor to modulate exon inclusion or skipping. Mol Cell. 2009;36 (6):996-1006. doi: 10.1016/j.molcel.2009.12.003. PubMed PMID:20064465 PubMed Central PMC2807993.
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