I study calcium-activated nonselective cation channels, situated in cardiomyocyte, that support important cellular response such as cardiac rhythmicity.
I have recently completed my MD-PhD in Professor Abriel’s lab, and I am currently working under as Postdoc.
I am continuing the experiments I started during my PhD and doing some advance research trying to answer the questions that came up in my previous studies.
My research focuses on TRPM4 related physiology and channelopathies in the heart. During my PhD study I was able to define a tool compound to study both mice and human TRPM4 activities. I am currently using this tool compound on mouse heart to understand the role of TRPM4 in cardiac physiology.
As my aspiration is to be a cardiac physician and I have a passion for business, I intend to combine the two starting my own pharmaceutical company in the future.
On the Web
Hypoxia Enhances Endothelial Intercellular Adhesion Molecule 1 Protein Level Through Upregulation of Arginase Type II and Mitochondrial Oxidative Stress. Liang, X., Arullampalam, P., Yang, Z. and Ming, X. Frontiers in Physiology, 14 August 2019. doi.org/10.3389/fphys.2019.01003
Pathological activation of CaMKII induces arrhythmogenicity through TRPM4 overactivation. Hu, Y., Kaschitza, D.R., Essers, M. et al. Pflugers Arch 2021 Mar; 473(3):507-519. doi: 10.1007/s00424-020-02507-w. Epub 2021 Jan 4.
Deletion of Trpm4 Alters the Function of the Nav1. 5 Channel in Murine Cardiac Myocytes. Ozhathil, L.C.; Rougier, J.-S.; Arullampalam, P.; Essers, M.C.; Ross-Kaschitza, D.; Abriel, H. Int. J. Mol. Sci. 2021, 22, 3401. doi.org/10.3390/ijms22073401
Species-Specific Effects of Cation Channel TRPM4 Small-Molecule Inhibitors. Arullampalam, P., Preti, B., Ross-Kaschitza, D., Lochner, M., Rougier, J-S, Abriel, H. Frontiers in Pharmacology, 12 July 2021. doi.org/10.3389/fphar.2021.712354