Heart failure arises from intrinsic diseases of cardiac muscle or idiopathic dilated cardiomyopathy as well as consequences of coronary artery disease after acute myocardial infarction and chronic ischemia. In patients with ST-segment–elevation myocardial infarction (MI) from a coronary thrombus, immediate reperfusion is the most effective therapy to prevent the loss of myocytes. The routine use of β-blockers, angiotensin inhibition therapy, and spironolactone blocks neurohormonal activation and prevents subsequent left ventricular (LV) remodeling. Stem cell therapy has emerged as an adjunctive approach to further attenuate postinfarction remodeling by stimulating myocyte proliferation and mitigating myocyte loss arising from within and outside of the infarct region. Despite favorable preclinical and early clinical studies in humans using bone marrow mononuclear cells, meta analyses of completed trials have failed to demonstrate a significant impact on clinical outcomes and LV function.1 Because substantial myocyte loss occurs during the first few days after infarction, the lack of efficacy may reflect delays in administering therapy that arise from synthesizing autologous cell products after the event. This and the increasing recognition of the role that paracrine effects play led to interest in allogeneic cells, such as cardiosphere-derived cells (CDCs) and mesenchymal stem cells (MSCs). These are relatively immune privileged and can be administered at the time of percutaneous coronary intervention and reperfusion. Cortical bone stem cells (CBSCs) are a particularly proliferative mesenchymal cell subtype2 that, in vitro, have characteristics similar to murine cKit+/Sca1+ cells and can to some extent transdifferentiate into cardiac myocytes.3 Enriching the cKit+ CBSC population could potentially provide an allogeneic cell therapy platform similar to cardiac stem cells (CSCs) without the need for a myocardial biopsy. Completed studies in nonreperfused murine infarct models have demonstrated that they attenuate postinfarction remodeling.3 Article, see p 1263 In this issue of …

中文翻译：

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皮质骨干细胞在再灌注时可减轻远端区域的心肌细胞重塑

心力衰竭源于心肌的内在疾病或特发性扩张型心肌病，以及急性心肌梗塞和慢性缺血后冠状动脉疾病的后果。对于患有冠状动脉血栓引起的ST段抬高型心肌梗死（MI）的患者，立即再灌注是防止心肌细胞丢失的最有效疗法。常规使用β受体阻滞剂，血管紧张素抑制疗法和螺内酯可阻断神经激素激活并防止随后的左心室（LV）重塑。干细胞疗法已经成为一种辅助方法，其通过刺激心肌细胞增殖和减轻由梗塞区域内外引起的心肌细胞损失来进一步减轻梗塞后重塑。尽管使用骨髓单个核细胞对人类进行了有益的临床前和早期临床研究，但已完成试验的荟萃分析未能证明对临床结局和左室功能有重大影响。1因为梗死后的头几天会发生大量的心肌细胞丢失，因此缺乏疗效的下降可能反映出事件发生后由于合成自体细胞产物而引起的治疗延迟。对旁分泌作用的作用的这种认识和日益增长的认识引起了对同种异体细胞（如心球来源的细胞（CDC）和间充质干细胞（MSC））的兴趣。这些具有相对免疫特权，可以在经皮冠状动脉介入治疗和再灌注时施用。皮质骨干细胞（CBSC）是一种特别增生的间充质细胞亚型2，在体外具有与鼠cKit + / Sca1 +细胞相似的特征，并且可以在某种程度上转分化为心肌细胞。3富集cKit + CBSC群体可以潜在地提供同种异体细胞类似于心脏干细胞（CSC）的治疗平台，无需进行心肌活检。对非再灌注鼠梗塞模型的完整研究表明，它们可以减轻梗塞后的重塑。3Article，see p 1263在本期… 3丰富cKit + CBSC群体可能会提供与心脏干细胞（CSC）类似的异体细胞治疗平台，而无需进行心肌活检。对非再灌注鼠梗塞模型的完整研究表明，它们可以减轻梗塞后的重塑。3Article，see p 1263在本期… 3丰富cKit + CBSC群体可能会提供与心脏干细胞（CSC）类似的异体细胞治疗平台，而无需进行心肌活检。对非再灌注鼠梗塞模型的完整研究表明，它们可以减轻梗塞后的重塑。3Article，see p 1263在本期…