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.
Recent Papers
- 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. 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.
- Bruyneel, A. et al. (2019). AlleleProfileR: A versatile tool to identify and profile sequence variants in edited genomes. PLoS One. 14(12): e0226694.
- Hurtado, C. et al. (2019). Disruption of NOTCH signaling by a small molecule inhibitor of the transcription factor RBPJ. Scientific Reports. 9(1):10811
- Hnatiuk, A. et al. (2019). Stars in the Night Sky: iPSC-Cardiomyocytes Return the Patient Context to Drug Screening. Cell Stem Cell. 24(4):506-507.
- Fang, M. et al. (2019). Small-Molecule Modulation of TDP-43 Recruitment to Stress Granules Prevents Persistent TDP-43 Accumulation in ALS/FTD. Neuron. S0896-6273(19)30524-0.
- Seeger, T. et al. (2019). A premature termination codon mutation in MYBPC3 causes hypertrophic cardiomyopathy via chronic activation of nonsense-mediated decay. Circ Res. 139(6):799-811
- Gómez-Galeno, JE. et al. (2018). b-Annulated 1,4-dihydropyridines as Notch inhibitors. Bioorg Med Chem Lett. 28(20):3363-3367.
- Bruyneel, AAN. et al. (2018). Will iPSC-cardiomyocytes revolutionize the discovery of drugs for heart disease?. Curr Opin Pharmacol. 42:55-61
- Cheng, J., et al. (2018). A novel inhibitor targets both Wnt signaling and ATM/p53 in colorectal cancer. Cancer Res. 78(17):5072-5083.
- Okolotowicz, KJ., et al. (2018). Novel tertiary sulfonamides as potent anti-cancer agents. Bioorg Med Chem. 26(15):4441-4451.
- Bruyneel, AAN., et al. (2018). Using iPSC Models to Probe Regulation of Cardiac Ion Channel Function. Curr Cardiol Rep. 25(7):57.
- Diez-Cuñado, M., et al. (2018). miRNAs that Induce Human Cardiomyocyte Proliferation Converge on the Hippo Pathway. Cell Rep. 23(7):2168-2174.
- Jeong, D., et al. (2018). miR-25 Tough Decoy Enhances Cardiac Function in Heart Failure. Mol Ther. 26(3):718-729.