Value Proposition:
- This technology provides a therapeutic approach for the regrowth of permanently damaged heart muscle.
- This could improve health outcomes for patients with severe heart failure.
Technology Description
Researchers at Johns Hopkins have discovered that the manipulation of circadian genes can induce the proliferation and regeneration of cardiomyocytes (cardiac muscle cells). Sympathetic neuron activity in the heart upregulates the production of period circadian (PER) proteins. PER proteins regulate mitosis in cardiomyocytes, inhibiting Cdk1 via the Wee1 kinase pathway. Inhibition of PER proteins allows cardiomyocytes to enter mitosis, which leads to increased proliferation and regeneration.
Unmet Need
Heart disease is the leading cause of death in the United States [1]. Heart failure arises when cardiomyocytes die (e.g., post-heart attack), as these cells have limited capacity for regeneration [2]. They are instead replaced by d by fibrous tissue, resulting in a gradual loss of heart function [3]. The standard-of-care in cases of severe heart failure is organ transplant [4], which carries significant risk [5]. There are no regenerative therapies currently available for heart failure. Therefore, there is a strong need to develop therapeutics aimed at cardiomyocyte regeneration to improve health outcomes for patients with heart failure.
Stage of Development
PER inhibition has been tested in healthy animal models and in cardiomyocytes in vitro; currently evaluating in animal models post-myocardial infarction and/or heart failure.
Publication
Tampakakis, E., Gangrade, H., Glavaris, S., Htet, M., Murphy, S., Lin, B. L., Liu, T., Saberi, A., Miyamoto, M., Kowalski, W., Mukouyama, Y. S., Lee, G., Minichiello, L., & Kwon, C. (2021). Heart neurons use clock genes to control myocyte proliferation. Science advances, 7(49), eabh4181. https://doi.org/10.1126/sciadv.abh4181
