Welcome to the Jenny Zhou Lab

Dr. Zhou has focused on translational research from the very beginning of her postgraduate study. To discover the molecular mechanisms and facilitate new therapeutic strategies for vascular diseases, Dr. Zhou has worked on angiogenesis and lymphangiogenesis, predominantly to investigate the role of CCM3, Trx2, SENP1 and AIP1 genes in animal models and in vitro for vascular biology, cell biology and signaling, as well as potential therapeutic targets which would provide promising treatment for vascular diseases such as cerebral cavernous malformation, diabetic retinopathy and cardiomyopathy.

In previous research, Dr. Zhou has:

1. Defined novel function of AIP1 and CCM3 in regulating VEGFR3 signaling in angiogenesis and lymphangiogenesis (Arterioscler Thromb Vasc Biol, 2014; Arterioscler Thromb Vasc Biol, 2021);
2. Elucidated critical function of mitochondrial redox protein Trx2 in cardiomyopathy in collaboration with Dr. Huang in the lab (Circulation, 2015), and found Trx2 modulates vessel sprouting and maturation in angiogenesis (ongoing work);
3. Demonstrated that SENP1 functions as an endogenous activator in VEGFR2 signalling by regulating VEGFR2 trafficking from the Golgi to endothelial cell surface which pathway plays a critical role in diabetes-associated angiogenesis (Nat Commun, 2018);
4. Established inducible endothelial-specific CCM3 mouse model for human cerebral cavernous malformation (CCM) disease and have intriguingly found that blockade of exocytosis or inhibition of Angpt2-TIE2 signaling completely blunts CCM lesion formation in the mouse model (Nat Med, 2016; Nat Commun, 2021).

This lab will continue to investigate the cardiovascular and retinal disease in the aspects of endothelial signaling and biology, vascular malformation and remodeling. The lab is conducting translational research in vascular biology with a focus on human vascular diseases like cerebral cavernous malformations (CCMs) and retinopathy. Our goal is to dissect the signaling pathways in endothelial cells involved in vascular development, remodeling and disease progression. We will use mouse genetic models, in vitro biochemical and cell biological approaches to define the critical molecules mediating vascular development and pathogenesis, to verify the signaling in human disease samples, and to identify therapeutic targets for human vascular diseases.