From molecular and cellular perspectives, heart failure is caused by the loss of cardiomyocytes—the fundamental contractile units of the heart. Because mammalian cardiomyocytes exit the cell cycle shortly after birth, the cardiomyocyte damage induced by myocardial infarction (MI) typically leads to dilatation of the left ventricle (LV) and often progresses to heart failure. However, recent findings indicate that the hearts of neonatal pigs completely regenerated the cardiomyocytes that were lost to MI when the injury occurred on postnatal day 1 (P1). This recovery was accompanied by increases in the expression of markers for cell-cycle activity in cardiomyocytes. These results suggest that the repair process was driven by cardiomyocyte proliferation. This review summarizes findings from recent studies that found evidence of cardiomyocyte proliferation in 1) the uninjured hearts of newborn pigs on P1, 2) neonatal pig hearts after myocardial injury on P1, and 3) the hearts of pigs that underwent apical resection surgery (AR) on P1 followed by MI on postnatal day 28 (P28). Analyses of cardiomyocyte single-nucleus RNA sequencing data collected from the hearts of animals in these three experimental groups, their corresponding control groups, and fetal pigs suggested that although the check-point regulators and other molecules that direct cardiomyocyte cell-cycle progression and proliferation in fetal, newborn, and postnatal pigs were identical, the mechanisms that activated cardiomyocyte proliferation in response to injury may differ from those that regulate cardiomyocyte proliferation during development.

中文翻译：

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促进大型哺乳动物心肌细胞增殖和心肌再生

从分子和细胞的角度来看，心力衰竭是由心肌细胞（心脏的基本收缩单位）的丧失引起的。由于哺乳动物心肌细胞在出生后不久就退出细胞周期，因此心肌梗塞（MI）引起的心肌细胞损伤通常会导致左心室（LV）扩张，并经常进展为心力衰竭。然而，最近的研究结果表明，新生猪的心脏完全再生了出生后第 1 天（P1）发生损伤时因心肌梗死而丢失的心肌细胞。这种恢复伴随着心肌细胞中细胞周期活性标记物表达的增加。这些结果表明修复过程是由心肌细胞增殖驱动的。本综述总结了最近的研究结果，这些研究发现 1) P1 新生猪未受伤的心脏、2) P1 心肌损伤后的新生猪心脏和 3) 接受心尖切除手术 (AR) 的猪的心脏存在心肌细胞增殖的证据。 ）在 P1，随后在产后第 28 天（P28）发生 MI。对这三个实验组动物、相应对照组和胎猪心脏收集的心肌细胞单核 RNA 测序数据的分析表明，尽管检查点调节因子和其他指导心肌细胞细胞周期进展和增殖的分子胎儿、新生和产后猪是相同的，响应损伤而激活心肌细胞增殖的机制可能与发育过程中调节心肌细胞增殖的机制不同。