Interdependent changes of nuclear lamins, nuclear pore complexes, and ploidy regulate cellular regeneration and stress response in the heart.

Interdependent changes of nuclear lamins, nuclear pore complexes, and ploidy regulate cellular regeneration and stress response in the heart.
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DOI:
10.1080/19491034.2023.2246310
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发表时间:
2023-12
期刊:
Nucleus (Austin, Tex.)
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其他
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在成年哺乳动物中,许多心肌细胞(心肌细胞)是多倍体,不增殖(有丝分裂后),因此不能促进心脏再生。相比之下,胎儿和新生儿心肌细胞是二倍体,增殖,并有助于心脏再生。我们已经确定了心肌细胞成熟过程中核板层、核孔复合体和DNA含量(倍性)的相互依赖的变化。这些结果为细胞如何改变其核转运以及细胞外信号对其基因调控的反应提供了新的视角。我们提出了如何改变核板层改变核孔复合物在心肌细胞。这些变化对心脏细胞再生和应激反应的后果进行了讨论。
In adult mammals, many heart muscle cells (cardiomyocytes) are polyploid, do not proliferate (post-mitotic), and, consequently, cannot contribute to heart regeneration. In contrast, fetal and neonatal heart muscle cells are diploid, proliferate, and contribute to heart regeneration. We have identified interdependent changes of the nuclear lamina, nuclear pore complexes, and DNA-content (ploidy) in heart muscle cell maturation. These results offer new perspectives on how cells alter their nuclear transport and, with that, their gene regulation in response to extracellular signals. We present how changes of the nuclear lamina alter nuclear pore complexes in heart muscle cells. The consequences of these changes for cellular regeneration and stress response in the heart are discussed.
靶向心脏中的CAMKII/ERK相互作用可防止心脏肥大。
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