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Chengjun Hu, MD, PhD


Chengjun Hu, MD, PhD

E-mail Address:

Office Address: 185# Donghu Road, Wuhan, Hubei, 430071


Associate Professor


Department of Anatomy

Research interests / Specialties:

Biology behavior of MSC and protein quality control and degradation.

Education and Training:

B.S., 1990-1995 Hubei Medical University, China

M.S., 1998-2001 Wuhan University, China

Ph.D., 2003-2009 Wuhan University, China

Visiting scholar, 2009 The Fukushima Medical University, Japan

Post-doctoral training, 2012-2014 The University of South Dakota, U.S.A

Research Description

My research investigate biology behavior of bone marrow stromal cells that long-term culture in vitro and protein changes of myocardial ischemia/ reperfusion injury.

For MSC, the work focus on the cell proliferation, differentiation, apoptosis, senescent and autophagy. We showed the different protein expressions in different terms.

For myocardial ischemia/reperfusion injury, we make myocardial ischemia/reperfusion injury models in over-expression / knock out ubiquilin mouse, then identify the changes of protein. Observe the ubiquitin and autophagy signal pathway in the injury model. So we can get further study in protein quality control and degradation.

Publication list

1. Hu, C.J., Wu, Y., Wan, Y., Wang, Q,, Song, J. (2008) Introduction of hIGF-1 gene into bone marrow stromal cells and its effects on the cell’s biological behaviors. Cell transplantation. 9, 1067-81.

2. Gao, Q.S., Hu C.J. (2009) Dynamic mortality factor model with conditional heteroskedasticity. Insurance: Mathematics and Economics. 3, 410-23.

3. Zheng, Y., Hu, C.J., Zhuo, R.H., Lei, Y.S., Han, N,N., He, L. (2014) Inhibition of autophagy alleviates the senescent state of MSCs during long-term culture. Mol Med Rep. 10,3003-8.

4. Lei, Y.S., Hu, C.J., Xu, H.X., Tian, Y.H. (2013) HPV16 infection regulates RASSF1A transcription mediated by p53. Mol Med Rep. 8,413-8.

5. Tian, ZW., Wang, C.H., Hu, C.J., Tian, Y.H., Liu, J.B., Wang, X.J. (2014)Autophagic-lysosomal inhibition compromises ubiquitin-proteasome system performance in a p62 dependent manner in cardio. PLoS One. 24;9(6):e100715.