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首页> 外文期刊>Heart, lung & circulation >Dissecting Molecular Mechanisms Underlying Pulmonary Vascular Smooth Muscle Cell Dedifferentiation in Pulmonary Hypertension: Role of Mutated Caveolin-1 (Cav1(F92A))-Bone Marrow Mesenchymal Stem Cells
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Dissecting Molecular Mechanisms Underlying Pulmonary Vascular Smooth Muscle Cell Dedifferentiation in Pulmonary Hypertension: Role of Mutated Caveolin-1 (Cav1(F92A))-Bone Marrow Mesenchymal Stem Cells

机译:肺动脉高压下肺血管平滑肌细胞消除术后分子机制:突变Caveolin-1(Cav1(F92A)) - 骨髓间充质干细胞的作用

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摘要

Background Pulmonary arterial hypertension (PAH) is characterised by remodelling in vascular smooth muscles, and switching from contractile (differentiated) to synthetic (dedifferentiated) phenotype. This study aimed to investigate the effect of a mutated caveolin-1 (Cav1(F92A)) gene from bone marrow mesenchymal stem cells (rBMSCs) on phenotypic switching in the smooth muscle cells during PAH.
机译:背景技术肺动脉高血压(PAH)的特征在于在血管平滑肌中重塑,并从收缩(分化)转换为合成(Deffifefeed)表型。 该研究旨在探讨突变的Caveolin-1(Cav1(F92a))基因从骨髓间充质干细胞(RBMSC)对PAH平滑肌细胞中的表型切换的影响。

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