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肺动脉高压的干细胞和祖细胞治疗:对右心室的影响(2013 年 Grover 会议系列)。

Stem and progenitor cell therapy for pulmonary arterial hypertension: effects on the right ventricle (2013 Grover Conference Series).

机构信息

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands ; Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, the Netherlands.

Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, the Netherlands.

出版信息

Pulm Circ. 2015 Mar;5(1):73-80. doi: 10.1086/679701.

DOI:10.1086/679701
PMID:25992272
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4405720/
Abstract

In experimental animals and in patients with pulmonary arterial hypertension (PAH), a wide spectrum of structural and functional conditions is known that may be responsible for the switch of a state of "compensated" right ventricular (RV) hypertrophy to a state of RV failure. In recent years, therapy with differentiated cells, endothelial progenitor cells, and mesenchymal stem cells has been shown to cause partial or complete reversal of pathological characteristics of PAH. The therapeutic effects of stem or progenitor cell therapy are considered to be (1) paracrine effects from stem or progenitor cells that had engrafted in the myocardium (or elsewhere), by compounds that have anti-inflammatory, antiapoptotic, and proangiogenic actions and (2) unloading effects on the right ventricle due to stem or progenitor cell-induced decrease in pulmonary vascular resistance and decrease in pulmonary artery pressure.

摘要

在实验动物和肺动脉高压(PAH)患者中,已知存在广泛的结构和功能状态,这些状态可能导致右心室(RV)代偿性肥厚向 RV 衰竭状态的转变。近年来,分化细胞、内皮祖细胞和间充质干细胞的治疗已被证明可以部分或完全逆转 PAH 的病理特征。干细胞或祖细胞治疗的治疗效果被认为是(1)来源于已经植入心肌(或其他部位)的干细胞或祖细胞的旁分泌作用,这些化合物具有抗炎、抗凋亡和促血管生成作用,以及(2)由于干细胞或祖细胞诱导的肺血管阻力降低和肺动脉压降低对右心室的卸载作用。

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本文引用的文献

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Mesenchymal stem cell trials for pulmonary diseases.间充质干细胞治疗肺部疾病的试验
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Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure.右心室肥厚向衰竭转变过程中的动态 microRNA 表达。
Physiol Genomics. 2012 May 1;44(10):562-75. doi: 10.1152/physiolgenomics.00163.2011. Epub 2012 Mar 27.
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