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I have a broad background in physiology, with specific training and expertise in research areas such as ion channel mechanisms, patch clamp electrophysiology, Mg homeostasis, mitochondria, and ER stress. I have carried out electrophysiological experiments to study nicotinic acetylcholine receptors at neuromuscular junctions, voltage-gated cardiac sodium channel and other cardiac ion channels. I have been working on different cardiac disease mouse models (hypertension, MI, HFpEF) and cell models (acutely isolated/cultured cardiomyocytes and human iPSC-derived cardiomyocytes). Recently, I am focusing on studying Mg deficiency-induced cardiac diastolic dysfunction (DD) and Mg supplementation on improvement of DD and HFpEF.
My research focuses on three projects. One is TRPM7 regulation on atrial fibrillation. TRPM7 is a Mg2+ transporter and could be a trigger for inflammation activation, mitochondrial ROS overproduction, and ER dysfunction in diabetes mellitus-associated AF. The second is magnesium deficiency on cardiac diastolic function (DD) and heart failure with preserved ejection fraction (HFpEF) by using a high fat diet-induced diabetic mouse model and a low-Mg diet-induced hypomagnesemia (HypoMg) mouse model. TRPM7 kinase plays a key role in HypoMg-mediated HFpEF. The third project is mitochondrial dysfunction in cardiac diastolic dysfunction on a diabetic mouse model. Mitochondrial targeted antioxidants have been tested in the diabetic mouse model to reverse cardiac diastolic dysfunction and future tests on larger animals are planned. The third project is the unfolded protein response and arrhythmias. Studies of electrophysiology, gene/protein expression, and in vivo animal tests show that the unfolded protein response mainly downregulates cardiac ion channels, causing electrical remodeling in ischemic heart failure.