Developing New Approaches to Treat Heart Disease
The Mercola laboratory is focused on developing new therapies for cardiovascular disease. Cardiovascular disease, including heart failure, remains a major cause of human mortality worldwide despite advances in clinical management. Our research combines in vitro disease models using cardiovascular cells generated from induced pluripotent stem cells (iPSCs) with high throughput screening to define disease mechanisms, identify drug targets and develop drug leads. Since iPSCs are derived from patient biopsies, these cells make it possible to visualize the effect of individual patient genetics on disease, and develop new and effective drugs.
Dr. Mercola is Professor of Cardiovascular Medicine and a member of the Stanford Cardiovascular Institute. He trained at the Dana-Farber Cancer Institute in Boston and Harvard Medical School. He was on the faculty at Harvard Medical School and then at the Sanford-Burnham-Prebys Medical Discovery Institute and the Department of Bioengineering at the University of California, San Diego prior to relocating to Stanford in 2015. The laboratory is funded by research grants from the National Institutes of Health (NIH), the California Institute for Regenerative Medicine and the Fondation Leducq.
Human cardiomyocytes derived from induced pluripotent stem cells (iPSCs) made from a healthy individual.
- McKeithan, W. et al. (2020). Reengineering an Antiarrhythmic Drug Using Patient hiPSC Cardiomyocytes to Improve Therapeutic Potential and Reduce Toxicity. Cell Stem Cell. 27, 1-9.
- Levitas, A. et al. (2020). A Novel Recessive Mutation in SPEG Causes Early Onset Dilated Cardiomyopathy. PLoS Genet. 16(9): e1009000.
- Briganti, F. et al. (2020). iPSC Modeling of RBM20-Deficient DCM Identifies Upregulation of RBM20 as a Therapeutic Strategy. Cell Reports. 32(10):108117.
- Feyen, D.A.M. et al. (2020). Metabolic Maturation Media Improve Physiological Function of Human iPSC-Derived Cardiomyocytes. Cell Reports. 32(3):107925.
- Vaskova, E. et al. (2020). Sacubitril/Valsartan Improves Cardiac Function and Decreases Myocardial Fibrosis Via Downregulation of Exosomal miR-181a in a Rodent Chronic Myocardial Infarction Model. J Am Heart Assoc. 9(13):e015640.
- Lu, S. et al. (2020). Hyperglycemia Acutely Increases Cytosolic Reactive Oxygen Species via O-linked GlcNAcylation and CaMKII Activation in Mouse Ventricular Myocytes. Circ Res. 126(10):e80-e96.