Urodele amphibians and some fish are capable of regenerating up to a quarter of their heart tissue after cardiac injury. While many anuran amphibians like Xenopus laevis are not capable of such feats, they are able to repair lesser levels of cardiac damage, such as that caused by oxidative stress, to a far greater degree than mammals. Using an optogenetic stress induction model that utilizes the protein KillerRed, we have investigated the extent to which mechanisms of cardiac regeneration are conserved during the restoration of normal heart morphology post oxidative stress in X. laevis tadpoles. We focused particularly on the processes of cardiomyocyte proliferation and dedifferentiation, as well as the pathways that facilitate the regulation of these processes. The cardiac response to KillerRed-induced injury in X. laevis tadpole hearts consists of a phase dominated by indicators of cardiac stress, followed by a repair-like phase with characteristics similar to mechanisms of cardiac regeneration in urodeles and fish. In the latter phase, we found markers associated with partial dedifferentiation and cardiomyocyte proliferation in the injured tadpole heart, which, unlike in regenerating hearts, are not dependent on Notch or retinoic acid signaling. Ultimately, the X. laevis cardiac response to KillerRed-induced oxidative stress shares characteristics with both mammalian and urodele/fish repair mechanisms, but is nonetheless a unique form of recovery, occupying an intermediate place on the spectrum of cardiac regenerative ability. An understanding of how Xenopus repairs cardiac damage can help bridge the gap between mammals and urodeles and contribute to new methods of treating heart disease.

中文翻译：

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从ROS诱导的压力中恢复非洲爪蟾心脏的方法利用了心脏再生的保守途径。

心脏受伤后，两栖动物和某些鱼类能够再生其心脏组织的四分之一。尽管像非洲爪蟾（Xenopus laevis）这样的许多无双栖动物两栖动物都无法做到这些壮举，但它们能够修复程度比哺乳动物低得多的心脏损伤，例如由氧化应激引起的心脏损伤。使用利用蛋白KillerRed的光遗传应激诱导模型，我们研究了X. laevis ad在氧化应激后恢复正常心脏形态的过程中，心脏再生机制得以保留的程度。我们特别关注心肌细胞增殖和去分化的过程，以及促进调节这些过程的途径。对KillerRed诱导的X损伤的心脏反应。laevis hearts的心脏由一个以心脏压力指示剂为主的阶段组成，其后是一个类似修复的阶段，其特征类似于乌德莱德鱼和鱼类的心脏再生机制。在后期阶段，我们发现与the受伤的心脏部分脱分化和心肌细胞增殖相关的标志物，与再生心脏不同，这些标志物不依赖于Notch或视黄酸信号传导。最终，X.laevis对KillerRed诱导的氧化应激的心脏反应与哺乳动物和urodele /鱼类修复机制均具有特征，但仍是一种独特的恢复形式，在心脏再生能力谱中占据中间位置。