Developing New Approaches to Treat Heart Disease
Human cardiomyocytes derived from induced pluripotent stem cells (iPSCs) made from a healthy individual.
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.
- Heygi, B., et. al. (2021). Cardiomyocyte Na+ and Ca2+ mishandling drives vicious cycle involving CaMKII, ROS, and ryanodine receptors. Basic Res. Cardiol. 116, 58.
- Chase, A. J., et. al. (2021). Highlights from Stanford Drug Discovery Symposium 2021. Cardiovasc. Res. 117 (10), e132–e134.
- Gomez-Galeno, J., et. al. (2021). Human-induced pluripotent stem cell-derived cardiomyocytes: Cardiovascular properties and metabolism and pharmacokinetics of deuterated mexiletine analogs. Pharmacol. res. perspect.
- Ji, M. et. al. (2021). The Present and Future of Mitochondrial-Based Therapeutics for Eye Disease. Transl. Vis. Sci. Technol. 10 (8), 4.
- Anselmo, A., et. al. (2021). Myocardial hypoxic stress mediates functional cardiac extracellular vesicle release. Eur. Heart. J. 42 (28), 2780–2792.
- Johnson, M., et. al. (2021). Human iPSC-derived Cardiomyocytes and Pyridyl-Phenyl Mexiletine Analogs. Bioorganic Med. Chem. Lett. 46, 2021, 128162.
- Cashman, J.R., et. al. (2021). Antiarrhythmic Hit to Lead Refinement in a Dish Using Patient-Derived iPSC Cardiomyocytes. J. Med. Chem. 64 (9), 5384-5403.
- Feyen, D., et. al. (2021). The Unfolded Protein Response as a Compensatory Mechanism and Potential Therapeutic Target in PLN R14del Cardiomyopathy. Circulation.
- Lei, Z., et. al. (2021). miR 132-212 Impairs Cardiomyocytes Contractility in the Failing Heart by Suppressing SERCA2a. Front Cardiovasc Med. 8, 592362.
- Hnatiuk, A., et. al. (2021). Human iPSC modeling of heart disease for drug development. Cell Chem Biol. 28 (3), 271-282.
- Chirikian, O., et. al. (2021). CRISPR/Cas9-based targeting of fluorescent reporters to human iPSCs to isolate atrial and ventricular-specific cardiomyocytes. Sci Rep. 11(1), 3026.
- Cheng, J., et. al. (2021). Small-molecule probe reveals a kinase cascade that links stress signaling to TCF/LEF and Wnt responsiveness. Cell Chem Biol. 28, 1-11.