{"title":"TRIM55 通过调节 Nrf2/HO-1 通路加剧心肌梗死后的心肌细胞凋亡","authors":"","doi":"10.1016/j.jacbts.2024.05.006","DOIUrl":null,"url":null,"abstract":"<div><div>Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro. The results showed that Trim55 knockout improved cardiac function and apoptosis after myocardial infarction, and overexpression aggravated cardiac function damage. The mechanism is that Trim55 interacts with nuclear factor, erythroid derived 2 (Nrf2) to accelerate its degradation and inhibit the expression of heme oxygenase 1, thereby promoting cardiomyocyte apoptosis.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002134/pdfft?md5=017379718d1c2bd24f63c67d39e1d9dd&pid=1-s2.0-S2452302X24002134-main.pdf","citationCount":"0","resultStr":"{\"title\":\"TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway\",\"authors\":\"\",\"doi\":\"10.1016/j.jacbts.2024.05.006\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro. The results showed that Trim55 knockout improved cardiac function and apoptosis after myocardial infarction, and overexpression aggravated cardiac function damage. The mechanism is that Trim55 interacts with nuclear factor, erythroid derived 2 (Nrf2) to accelerate its degradation and inhibit the expression of heme oxygenase 1, thereby promoting cardiomyocyte apoptosis.</div></div>\",\"PeriodicalId\":14831,\"journal\":{\"name\":\"JACC: Basic to Translational Science\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":8.4000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2452302X24002134/pdfft?md5=017379718d1c2bd24f63c67d39e1d9dd&pid=1-s2.0-S2452302X24002134-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JACC: Basic to Translational Science\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2452302X24002134\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JACC: Basic to Translational Science","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2452302X24002134","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway
Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro. The results showed that Trim55 knockout improved cardiac function and apoptosis after myocardial infarction, and overexpression aggravated cardiac function damage. The mechanism is that Trim55 interacts with nuclear factor, erythroid derived 2 (Nrf2) to accelerate its degradation and inhibit the expression of heme oxygenase 1, thereby promoting cardiomyocyte apoptosis.
期刊介绍：
JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.
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