Recently, the reporter of Science and Technology Daily learned from Harbin Medical University that the team of Yang Baofeng, an academician of the CAE Member and a professor of the School of Pharmacology of Harbin Medical University, found for the first time that the interaction between p53 and ASPP1 proteins can reduce myocardial cell damage. Relevant research results were published in the international journal Circulation Research. Yang Baofeng and his team members, Professor Pan Zhenwei and Professor Lv Yanjie, found that in the normal heart, there are very few p53 and ASP1 proteins, but when myocardial ischemia and reperfusion occurs, these two proteins will increase in large numbers, and enter the nucleus from the cytoplasm to stimulate the cell death process. The team found that when the expression of one of the proteins was artificially inhibited, the transport of the other protein to the nucleus was blocked, and cell death was reduced; On the contrary, when the expression of one protein is increased, the transport of the other protein into the nucleus increases, and cell death increases. This phenomenon suggests that these two proteins need to be combined in the cytoplasm and enter the nucleus "hand in hand" before activating the cell death process. The team designed a polypeptide molecule that can prevent the binding of p53 and ASP1 proteins, and found that it can significantly inhibit the transport of p53 and ASP1 proteins into the nucleus, and reduce myocardial cell damage. This finding suggests that interfering with the interaction of p53 and ASP1 protein can be a new strategy for the development of myocardial protective drugs. Next, Yang Baofeng's team will further optimize the polypeptide molecules that affect the interaction of p53 and ASP1 proteins, and design new compounds that inhibit the combination of the two, aiming to finally develop new drugs for clinical myocardial protection. (Outlook New Era)
Edit：qihang Responsible editor：xinglan
Source：http://digitalpaper.stdaily.com/http_www.kjrb.com/kjrb/html/2023-01/18/content_547632.htm?div=-1
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