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用于心肌缺血的CD34+细胞移植

Transplantation of CD34+ cells for myocardial ischemia.

作者信息

Matta Anthony, Nader Vanessa, Galinier Michel, Roncalli Jerome

机构信息

Department of Cardiology, Institute CARDIOMET, University Hospital of Toulouse, Toulouse 31059, France.

出版信息

World J Transplant. 2021 May 18;11(5):138-146. doi: 10.5500/wjt.v11.i5.138.

DOI:10.5500/wjt.v11.i5.138
PMID:34046316
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8131931/
Abstract

CD34+ cells are multipotent hematopoietic stem cells also known as endothelial progenitor cells and are useful in regenerative medicine. Naturally, these cells are mobilized from the bone marrow into peripheral circulation in response to ischemic tissue injury. CD34+ cells are known for their high proliferative and differentiation capacities that play a crucial role in the repair process of myocardial damage. They have an important paracrine activity in secreting factors to stimulate vasculogenesis, reduce endothelial cells and cardiomyocytes apoptosis, remodel extracellular matrix and activate additional progenitor cells. Once they migrate to the target site, they enhance angiogenesis, neovascularization and tissue regeneration. Several trials have demonstrated the safety and efficacy of CD34+ cell therapy in different settings, such as peripheral limb ischemia, stroke and cardiovascular disease. Herein, we review the potential utility of CD34+ cell transplantation in acute myocardial infarction, refractory angina and ischemic heart failure.

摘要

CD34+细胞是多能造血干细胞,也被称为内皮祖细胞,在再生医学中很有用。自然情况下,这些细胞会响应缺血性组织损伤,从骨髓动员到外周循环中。CD34+细胞以其高增殖和分化能力而闻名,这些能力在心肌损伤的修复过程中起着关键作用。它们在分泌因子以刺激血管生成、减少内皮细胞和心肌细胞凋亡、重塑细胞外基质以及激活其他祖细胞方面具有重要的旁分泌活性。一旦它们迁移到靶位点,就会增强血管生成、新血管形成和组织再生。多项试验已证明CD34+细胞疗法在不同情况下的安全性和有效性,如外周肢体缺血、中风和心血管疾病。在此,我们综述CD34+细胞移植在急性心肌梗死、难治性心绞痛和缺血性心力衰竭中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/822a/8131931/842531a01f2e/WJT-11-138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/822a/8131931/842531a01f2e/WJT-11-138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/822a/8131931/842531a01f2e/WJT-11-138-g001.jpg

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