Cutie Stephen, Huang Guo N
Cardiovascular Research Institute and Department of Physiology, University of California, San Francisco, San Francisco, CA, 94158, USA.
Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA, 94158, USA.
Cell Regen. 2021 Mar 1;10(1):6. doi: 10.1186/s13619-020-00068-y.
Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury - as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.
心脏再生是脊椎动物的一种原始特征，随着近代脊椎动物谱系进化以适应新环境和选择压力，以及某些物种的成员在发育过程中向成年形态发展，这种特征逐渐丧失。虽然像人类和啮齿动物这样的高等脊椎动物成年后通过永久性纤维化和心输出量丧失来解决心脏损伤，但这些相同物种的新生儿在受伤后可以完全再生心脏结构和功能——许多硬骨鱼和有尾两栖动物等成年低等脊椎动物也可以。最近的研究阐明了几个广泛的因素，这些因素被认为在进化和发育过程中导致了心脏再生潜力的丧失：富氧环境、脊椎动物的产热、复杂的适应性免疫系统以及癌症风险权衡。在这篇综述中，我们讨论了这些假设的证据，以及它们在脊椎动物心脏再生过程中起作用的细胞参与者和分子调节因子。
