动物实验 z-bo 2020-08-19 516

　　This discovery provides the possibility of using drugs that mimic the gene silencing molecule, a microRNA or small RNA, to regenerate myocardium and treat heart disease. Unlike other organs, the adult heart lacks the ability to form new cells and repair damage after injury. Prior to the recent discovery, mammalian hearts did not appear to regenerate; these findings suggest that mice can regenerate cardiomyocytes (cardiomyocytes) for up to 6 days after birth.

　　YingTian and colleagues want to know whether miR302-367 (a group of microRNA) can be used to restore this regenerative ability in adult mice; whether miR302-367 is suitable for mammals, including human proliferation, which can drive cells in embryonic development. They found that in newborn mice, the overexpression of this microRNA promotes the proliferation of cardiomyocytes, while its deletion reduces the growth of cardiomyocytes. NA sequencing showed that miR302-367 can block genes in the Hippo signaling pathway; this pathway acts as a molecular gate that prevents cell division. By "releasing" this molecular gate, miR302-367 can induce cardiomyocytes to re-enter the cell cycle and proliferate. Activating microRNA in adult mice with myocardial infarction can stimulate small fragments of new cell growth, reduce scarring, and repair damaged myocardial tissue. However, the overexpression of this microRNA can increase the risk of cell proliferation, leading to cardiac hypertrophy and eventually heart failure. Short-term treatment with miR302-367 mimics can heal the damaged tissues of mice while avoiding these side effects.