Myocyte proliferation in end-stage cardiac failure in humans
Myocyte proliferation in end-stage cardiac failure in humans
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DOI：
10.1073/pnas.95.15.8801
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发表时间：
1998-07-21
影响因子：
11.1
通讯作者：
Anversa, P
中科院分区：
文献类型：
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作者：
Kajstura, J;Leri, A;Anversa, P
几十年前提出的教条坚持认为心肌细胞是终末分化的细胞，并且在成人心脏中不可能分裂。最近，偶尔可以看到心肌细胞中的核有丝分裂，但这些观察结果受到质疑，因为假设细胞增殖的速度对实际的组织再生无关紧要。此外，在正常心肌中未检测到有丝分裂。然而，对常规组织学准备的分析构成了肌细胞无法重新进入细胞周期和分裂的信念的基础，忽略了这些技术的局限性。我们在这里通过共聚焦显微镜报告，在对照人类心脏中，每100万个肌细胞中有14个处于有丝分裂状态。在终末期缺血性心脏病（每百万152个肌细胞）和特发性扩张型心肌病（每百万131个肌细胞）中，该参数增加了近10倍。由于左心室含有5.8 × 10(9)个肌细胞，这些有丝分裂指标提示对照心脏和缺血性和特发性扩张型心肌病心脏的整个心室心肌分别有81.2 × 10(3)、882 × 10(3)和760 × 10(3)个肌细胞处于有丝分裂状态，且有丝分裂持续时间不超过1小时，提示随着时间的推移，非病理性和病理性心脏均可形成大量肌细胞。获得了肌细胞胞质分裂的证据，为肌细胞增殖提供了明确的证据。
Introduced several decades ago, the dogma persists that cardiac myocytes are terminally differentiated cells and that division of muscle tells is impossible in the adult heart, More recently, nuclear mitotic divisions in myocytes occasionally were seen, but those observations were challenged on the assumption that the rate of cell proliferation was inconsequential for actual tissue regeneration. Moreover, mitoses were never detected in normal myocardium. However, the analysis of routine histologic preparations constituted the basis for the belief that myocytes were unable to reenter the cell cycle and divide, ignoring the limitations of these techniques, We report here by confocal microscopy that 14 myocytes per million were in mitosis in control human hearts, A nearly 10-fold increase in this parameter was measured in end-stage ischemic heart disease (152 myocytes per million) and in idiopathic dilated cardiomyopathy (131 myocytes per million). Because the left ventricle contains 5.8 x 10(9) myocytes, these mitotic indices imply that 81.2 x 10(3), 882 x 10(3), and 760 x 10(3) myocytes were in mitosis in the entire ventricular myocardium of control hearts and hearts affected by ischemic and idiopathic dilated cardiomyopathy, respectively, Additionally, mitosis lasts less than 1 hr, suggesting that large numbers of myocytes can be formed in the nonpathologic and pathologic heart with time. Evidence of cytokinesis in myocytes was obtained, providing unequivocal proof of myocyte proliferation.