期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2023.1181515
关键词
miR-182; atherosclerosis; myocardial; ischemia; ischemic stroke; heart failure; mesenchymal stromal cells; ischemia/reperfusion (I/R) injury
In recent decades, the treatment of cardiovascular and cerebrovascular diseases has advanced greatly, leading to more effective prevention of cardiovascular and cerebrovascular events. However, cardiac and cerebral atherothrombotic complications still cause significant morbidity and mortality worldwide. This article discusses the role of miR-182 in regulating various factors related to atherosclerosis, coronary artery disease, myocardial infarction, ischemia/reperfusion injury, organ transplant, cardiac hypertrophy, hypertension, heart failure, congenital heart disease, and cardiotoxicity. Additionally, it summarizes the current progress of miR-182 therapeutics in clinical development and highlights challenges that need to be addressed for clinical application in patients with cardiac disease.
The treatment of cardiovascular and cerebrovascular diseases have undergone major advances in recent decades, allowing for a more effective prevention of cardiovascular and cerebrovascular events. However, cardiac and cerebral atherothrombotic complications still account for substantial morbidity and mortality worldwide. Novel therapeutic strategies are critical to improve patient outcomes following cardiovascular diseases. miRNAs are small non-coding RNAs, that regulate gene expression. Here, we discuss the role of miR-182 in regulating myocardial proliferation, migration, hypoxia, ischemia, apoptosis and hypertrophy in atherosclerosis, CAD, MI, I/R injury, organ transplant, cardiac hypertrophy, hypertension, heart failure, congenital heart disease and cardiotoxicity. Besides, we also summarize the current progress of miR-182 therapeutics in clinical development and discuss challenges that will need to be overcome to enter the clinic for patients with cardiac disease.
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