FGF induces hypertrophy and angiogenesis in hibernating myocardium.
FGF induces hypertrophy and angiogenesis in hibernating myocardium.
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DOI：
10.1161/01.res.0000164184.63158.6c
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发表时间：
2005-04
影响因子：
20.1
通讯作者：
S. Vatner
中科院分区：
文献类型：
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作者：
S. Vatner
请参阅相关文章，第 767-775 页 多年来，人们对通过各种生长因子刺激血管生成非常感兴趣，包括成纤维细胞生长因子 (FGF) 家族。 FGF-5 是一种原癌基因，已知可刺激包括癌症在内的多种细胞类型的细胞生长和增殖。1 心肌细胞还可以产生不同的 FGF 同工型，例如，已表明冬眠心肌中碱性 FGF 的表达增加，2 这是《循环研究》中发表的当前研究感兴趣的疾病状态。3 FGF-5 在心脏中最常被引用的作用是促进血管生成。多项研究表明，心脏中 FGF-5 的基因转移可增加血管形成和局部血流量。4-6 这种效应是由心肌细胞产生 FGF-5，然后将其释放到细胞外空间来介导的。此外，FGF-5 可以作为心脏细胞生长的自分泌/旁分泌机制，并作为针对不可逆缺血性损伤的细胞保护机制。7 事实上，之前对 FGF 作用的大部分兴趣都集中在血管生成领域，其中慢性缺血的猪模型已被证明可以通过血管生成增加血流量。4-6,8-10 相反，Suzuki 等人的文章3 得出的结论是，用FGF 改善了猪冬眠心肌模型的功能，但其有益作用的机制涉及“刺激肥大和少数心肌细胞重新进入细胞周期的有丝分裂期，而不是血管生成……”3 这些观察结果在概念上很重要，因为之前治疗慢性缺血性心肌的研究重点是血管生成，而不是通过……来改善功能。
See related article, pages 767–775 For several years there has been considerable interest in stimulating angiogenesis by a variety of growth factors, including the family of fibroblast growth factors (FGF). FGF-5 is a protooncogene known to stimulate cell growth and proliferation in multiple cell types, including cancer.1 The cardiac myocyte can also produce different isoforms of FGFs, eg, it has been shown that the expression of basic FGF increases in hibernating myocardium,2 which was the disease state of interest in the current study published in Circulation Research .3 The most commonly cited effect of FGF-5 in the heart is to promote angiogenesis. Several studies have shown that gene transfer of FGF-5 in the heart increases vessel formation and regional blood flow.4–6 This effect is mediated by a production of FGF-5 by the cardiac myocytes, followed by its release in the extracellular space. In addition, FGF-5 can function as an autocrine/paracrine mechanism of cardiac cell growth and as a cytoprotective mechanism against irreversible ischemic damage.7 Indeed, most of the prior interest on the role of FGF has been in the field of angiogenesis, where swine models of chronic ischemia have been shown to increase blood flow, presumably through angiogenesis.4–6,8–10 In contrast, the article by Suzuki et al,3 concluded that gene therapy with FGF improved function in their swine model of hibernating myocardium, but the mechanism of the salutary effect involved “rather than angiogenesis, stimulation of hypertrophy and re-entry of a small number of myocytes into the mitotic phase of the cell cycle… ”3 These observations are conceptually important in that the focus of prior studies on treating chronically ischemic myocardium has been on angiogenesis, and not directed at improving function through …