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DOI 10.1089/scd.2021.0006

Медицинская библиотека · Stem cells and development · 2021

The Vital Roles of Mesenchymal Stem Cells and the Derived Extracellular Vesicles in Promoting Angiogenesis After Acute Myocardial Infarction.

Zhang Li-Li, Xiong Yu-Yan, Yang Yue-Jin

СтатьяПоддержка исследования: вне правительства СШАОбзорПеревод в очереди

Аннотация

Acute myocardial infarction (AMI) is an event of ischemic myocardial necrosis caused by acute coronary artery occlusion, which ultimately leads to a large loss of cardiomyocytes. The prerequisite of salvaging ischemic myocardium and improving cardiac function of patients is to provide adequate blood perfusion in the infarcted area. Apart from reperfusion therapy, it is also urgent and imperative to promote angiogenesis. Recently, growing evidence based on promising preclinical data indicates that mesenchymal stem cells (MSCs) can provide therapeutic effects on AMI by promoting angiogenesis. Extracellular vesicles (EVs), membrane-encapsulated vesicles with complex cargoes, including proteins, nucleic acids, and lipids, can be derived from MSCs and represent part of their functions, so EVs also possess the ability to promote angiogenesis. However, poor control of the survival and localization of MSCs hindered clinical transformation and made scientists start looking for new approaches based on MSCs. Identifying the role of MSCs and their derived EVs in promoting angiogenesis can provide a theoretical basis for improved MSC-based methods, and ultimately promote the clinical treatment of AMI. This review highlights potential proangiogenic mechanisms of transplanted MSCs and the derived EVs after AMI and summarizes the latest literature concerning the novel methods based on MSCs to maximize the angiogenesis capability.

Для цитирования: Zhang Li-Li, Xiong Yu-Yan, Yang Yue-Jin. The Vital Roles of Mesenchymal Stem Cells and the Derived Extracellular Vesicles in Promoting Angiogenesis After Acute Myocardial Infarction.. Stem cells and development. 2021. DOI: 10.1089/scd.2021.0006.

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