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血管新生:间充质干细胞治疗缺血性心脏病的主要机制

Neovascularization: The Main Mechanism of MSCs in Ischemic Heart Disease Therapy.

作者信息

Shi Weili, Xin Qiqi, Yuan Rong, Yuan Yahui, Cong Weihong, Chen Keji

机构信息

Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

National Clinical Research Center for Chinese Medicine Cardiology, Beijing, China.

出版信息

Front Cardiovasc Med. 2021 Jan 26;8:633300. doi: 10.3389/fcvm.2021.633300. eCollection 2021.

DOI:10.3389/fcvm.2021.633300
PMID:33575274
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7870695/
Abstract

Mesenchymal stem cell (MSC) transplantation after myocardial infarction (MI) has been shown to effectively limit the infarct area in numerous clinical and preclinical studies. However, the primary mechanism associated with this activity in MSC transplantation therapy remains unclear. Blood supply is fundamental for the survival of myocardial tissue, and the formation of an efficient vascular network is a prerequisite for blood flow. The paracrine function of MSCs, which is throughout the neovascularization process, including MSC mobilization, migration, homing, adhesion and retention, regulates angiogenesis and vasculogenesis through existing endothelial cells (ECs) and endothelial progenitor cells (EPCs). Additionally, MSCs have the ability to differentiate into multiple cell lineages and can be mobilized and migrate to ischemic tissue to differentiate into ECs, pericytes and smooth muscle cells in some degree, which are necessary components of blood vessels. These characteristics of MSCs support the view that these cells improve ischemic myocardium through angiogenesis and vasculogenesis. In this review, the results of recent clinical and preclinical studies are discussed to illustrate the processes and mechanisms of neovascularization in ischemic heart disease.

摘要

在众多临床和临床前研究中,心肌梗死(MI)后间充质干细胞(MSC)移植已被证明能有效限制梗死面积。然而,MSC移植治疗中与此活性相关的主要机制仍不清楚。血液供应是心肌组织存活的基础,而形成有效的血管网络是血流的先决条件。MSC的旁分泌功能贯穿于新生血管形成过程,包括MSC动员、迁移、归巢、黏附和滞留,通过现有的内皮细胞(EC)和内皮祖细胞(EPC)调节血管生成和血管发生。此外,MSC有能力分化为多种细胞谱系,并且可以被动员并迁移到缺血组织,在一定程度上分化为EC、周细胞和平滑肌细胞,这些都是血管的必要组成部分。MSC的这些特性支持了这样一种观点,即这些细胞通过血管生成和血管发生改善缺血心肌。在这篇综述中,讨论了近期临床和临床前研究的结果,以阐明缺血性心脏病中新生血管形成的过程和机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca7/7870695/d12a36b5d2d3/fcvm-08-633300-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca7/7870695/295f74b6d8e4/fcvm-08-633300-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca7/7870695/d12a36b5d2d3/fcvm-08-633300-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca7/7870695/295f74b6d8e4/fcvm-08-633300-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eca7/7870695/d12a36b5d2d3/fcvm-08-633300-g0002.jpg

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本文引用的文献

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Mesenchymal Stem Cells Promote the Resolution of Cardiac Inflammation After Ischemia Reperfusion Via Enhancing Efferocytosis of Neutrophils.间质干细胞通过增强中性粒细胞的吞噬作用促进缺血再灌注后心肌炎症的消退。
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源自不同组织的间充质干细胞治疗效果比较表明,在治疗急性心肌梗死中,抗细胞凋亡比血管生成更关键。
Stem Cell Res Ther. 2025 May 13;16(1):236. doi: 10.1186/s13287-025-04378-3.
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N-CADHERIN/CD168 subpopulation determines therapeutic variations of UC-MSCs for cardiac repair after myocardial infarction.N-钙黏蛋白/CD168 亚群决定了 UC-MSCs 在心肌梗死后心脏修复中的治疗变异性。
Stem Cell Res Ther. 2024 Nov 13;15(1):423. doi: 10.1186/s13287-024-04032-4.
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