Save the heart and refuse the infarction!

Release date: 2015-04-14

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The heart of newborn mice is regenerated by cardiomyocyte proliferation after being damaged, but after a week, this self-repairing ability will disappear significantly. Studies have shown that neuregulin 1 (NRG1) can promote cardiac regeneration and become a therapeutic strategy for the treatment of heart damage.

Scientists from Israel have found that the NRG1 co-receptor ERBB2 is very important for cardiac repair in the case of cardiac injury. ERBB2 can induce myocardial cell degeneration, proliferation, re-differentiation and regeneration to complete myocardial repair. Recently, the results of this study were published online in the international academic journal nature cell biology.

In this study, the researchers used the function-deficient and functionally acquired gene tools to explore the role of the co-receptor ERBB2 of NRG1 in cardiac regeneration. They found that NRG1-induced cardiomyocyte proliferation disappeared after one week of birth, mainly due to inhibition of ERBB2 expression. Specific knockout of ERBB2 in cardiomyocytes found that ERBB2 is important for cardiomyocyte regeneration in the embryonic/neonatal stage. The researchers also constitutively expressed ERBB2 in cardiomyocytes of newborn mice, young mice and adult mice, and found that this led to cardiac hypertrophy, mainly due to hypertrophy of cardiomyocytes, dedifferentiation and cell proliferation. These three processes are regulated by ERK, AKT and GSK3β/β-catenin signaling pathways, respectively. The researchers also found that transient induction of ERBB2 expression after myocardial infarction triggers dedifferentiation and proliferation of cardiomyocytes, followed by re-differentiation and regeneration to achieve cardiac damage repair.

This study demonstrates that the NRG1 co-receptor ERBB2 is essential for cardiomyocyte dedifferentiation and cell proliferation in the context of cardiac injury, and can reactivate the proliferation and regenerative potential of postnatal mouse cardiomyocytes, and is a treatment for myocardial infarction and other cardiac damage diseases. An important potential target.

Source: Bio Valley

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