miR-17-92 as targets and agents for cardiac regeneration
Inventors: Dazhi Wang, Jinghai Chen
Invention Types: Therapeutics
Research Areas: Cardiovascular/Cardiology
Keywords: Cell Therapy, Heart DiseaseFor More Information Contact: Miracco, Amy
Cardiomyocytes in adult mammalian hearts are terminally differentiated and lack the capacity to regenerate. Death of cardiomyocytes are primary causes of heart failure and mortality. An ability to regenerate heart tissues could bring a valuable new treatment for patients. |
Dr. Da Zhi Wang and Dr. Jinghai Chen identified miR-17-92 as a critical regulator of cardiomyocyte proliferation. The researchers found that overexpression of miR-17-92 induces cardiomyocyte proliferation in embryonic, postnatal, and adult hearts. They identified that miR-19, in particular, is required for and sufficient to induce cardiomyocyte proliferation in vitro, and in vivo experiments are underway to further validate the initial results. The researchers also identified PTEN, a tumor suppressor, as a miR-17-92 target to mediate the function of miR-17-92 in cardiomyocyte proliferation.
These studies suggest that miR-17-92 cluster have the potential to be therapeutic targets and agents for cardiac repair and heart regeneration.
Death of mature cardiomyocytes in pathological cardiac conditions and the lack of regeneration capacity of adult hearts are primary causes of heart failure and mortality. miR-17-92 is required for cardiomyocyte proliferation in the heart.
miR-17-92 induces cardiomyocyte proliferation in embryonic, postnatal and adult hearts, and itâ€™s over expression protects the heart from myocardial infarction-induced injury.
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Key Publications: Chen J, Huang ZP, Seok HY, Ding J, Kataoka M, Zhang Z, Hu X, Wang G, Lin Z,
Wang S, Pu WT, Liao R, Wang DZ. mir-17-92 cluster is required for and sufficient to induce cardiomyocyte proliferation in postnatal and adult hearts. Circ Res. 2013 Jun 7;112(12):1557-66. doi: .1161/CIRCRESAHA.112.300658. Epub 2013 Apr 10. PubMed PMID: 23575307.
IPStatus: Pat. Pend.