Telomere attrition in cardiomyocytes is associated with decreased contractility, cellular senescence, and up-regulation of proapoptotic transcription factors. Pim1 is a cardioprotective kinase that antagonizes the aging phenotype of cardiomyocytes and delays cellular senescence by maintaining telomere length, but the mechanism remains unknown. Another pathway responsible for regulating telomere length is the transforming growth factor beta (TGFβ) signalling pathway where inhibiting TGFβ signalling maintains telomere length. The relationship between Pim1 and TGFβ has not been explored. This study delineates the mechanism of telomere length regulation by the interplay between Pim1 and components of TGFβ signalling pathways in proliferating A549 cells and post-mitotic cardiomyocytes.

中文翻译：

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Pim1 通过抑制 TGFβ 信号传导维持小鼠心肌细胞的端粒长度。

心肌细胞的端粒磨损与收缩性降低、细胞衰老和促凋亡转录因子的上调有关。Pim1 是一种心脏保护激酶，可通过维持端粒长度来拮抗心肌细胞的衰老表型并延缓细胞衰老，但其机制仍不清楚。另一个负责调节端粒长度的途径是转化生长因子 β (TGFβ) 信号通路，其中抑制 TGFβ 信号可以维持端粒长度。Pim1 和 TGFβ 之间的关系尚未探索。本研究通过 Pim1 和 TGFβ 信号通路成分在增殖的 A549 细胞和有丝分裂后心肌细胞中的相互作用，描述了端粒长度调节的机制。