University Hospital of Ferrara, Cotignola, Ravenna, Italy.
Circ J. 2009 Nov;73(11):1973-82. doi: 10.1253/circj.cj-09-0573. Epub 2009 Oct 10.
Remodeling myocytes show a typical switch between the embryonic and classical features of apoptosis and/or hypertrophy representing a signal of death (ie, apoptosis) and a signal of life (ie, hypertrophy). The adult myocyte, however, is a terminal cell; usually it is unable to reproduce and death is not genetically programmed (apoptosis), but occurs by necrosis. The reinstatement of apoptosis and development of hypertrophy during remodeling could be part of the switch forward to the embryonic phenotype with reinstatement of the early embryonic genetic program. Hypertrophy and apoptosis are "sons" of the same "mother": the local, tissue neuroendocrine-neurohumoral response to a mechanical stretch of the myocytes consequent to the geometric changes imposed on the viable myocytes by the necrotic ones. As expected, the life and death cycle is very closely regulated by several autocrine systems, one of which is linked to the interleukin-6 family via a regulatory protein named GP-130. Activation of the GP-130 slows down the death signals, thus favoring hypertrophy and reducing fibrosis.
重塑的心肌细胞表现出典型的胚胎特征和经典凋亡特征和/或肥大之间的转换，代表死亡信号（即凋亡）和生命信号（即肥大）。然而，成年心肌细胞是终末细胞；通常，它无法复制，死亡不是遗传编程的（凋亡），而是坏死。重塑过程中凋亡的重新激活和肥大的发展可能是向前向胚胎表型转换的一部分，重新激活早期胚胎遗传程序。肥大和凋亡是同一个“母亲”的“儿子”：局部组织神经内分泌神经激素对心肌细胞的机械拉伸的反应，继而导致坏死心肌细胞对存活心肌细胞施加的几何变化。不出所料，生与死的循环受到多种自分泌系统的严格调控，其中一个系统通过一种名为 GP-130 的调节蛋白与白细胞介素 6 家族相关联。GP-130 的激活减缓了死亡信号，从而有利于肥大并减少纤维化。
