Jingxiong Wang, PhD

Dr. Wang’s training and working experience have equipped him to be able to carry out highly challenging translational research projects. The primary aim of his research is to delineate the mechanisms by which modulation of some potassium channels can significantly impact the development and therapy of cardiovascular and neuronal diseases. Dr. Wang’s specific long-term goal is to translate the Kv7/M-channel modulator into epilepsy and the Kv1.3-channel modulator into chemobrain for clinical therapy.

Over the last 15 years, he has worked as a key investigator conducting several translational research projects. In the project “Doxorubicin (DOX)-induced Cardiotoxicity: The Role of Topoisomerase 2B” (HL126916), Dr. Wang developed expertise to create tumor models in mice and assess the efficacy of a variety of chemotherapy including treating transplanted breast cancer with combination of Doxorubicin plus Dexrazoxane, leading to the clinical trial “Prevention of Heart Failure induced by Doxorubicin with Early Administration of Dexrazoxane” (HL051993). In the project “Molecular Imaging of Stem Cell Transplantation in the Heart” (HL086983), he developed and validated multimodality (MRI/CT/PET/BLI) molecular imaging techniques and verified that human CD34+ cells can enhance angiogenesis responsible for functional improvement for the infarcted heart. Dr. Wang’s most challenging project has been to explore a mouse model phenotyping in Sudden Unexpected Death in Epilepsy (SUDEP). His insights in conveying bench research into clinical applications for complex diseases allows Dr. Wangto lead and coordinate a group of researchers to explicate the cause of SUDEP in the mouse model, which discovered that the hyper-SUMOylation of a potassium channel KV7 in hippocampal neurons is responsible for SUDEP.

Over the last two years, Dr. Wang has worked closely with Dr. De-Pei Li to conceive and conduct the proposed project, in which we found that DOX treatment induced cognitive impairment, elevated Kv1.3 protein levels, reduced long-term potentiation (LTP), and activated microglia in the hippocampus. Administration of Kv1.3 channel-specific blocker PAP-1 significantly mitigated cognitive impairment, synaptic dysfunction, and microglia activation in the DOX-treated mice. In our ongoing and future studies, Dr. Wang’s expertise will target Kv1.3 channels to determine mechanistically that the DOX-induced neurocognitive dysfunction can be mitigated with the Kv1.3 channel blocker PAP-1 in animal models, and ultimately, translate the findings in the animal research to the clinic.