2017年11月20日 · Mechanistically, we found cardiac myocyte miR-29 to de-repress Wnt signaling by directly targeting four pathway factors. Our data suggests that, cell- or tissue-specific antimiR-29 delivery may...

2025年2月14日 · Using NRCM lacking Pontin (by siRNA transfection) we observed that MST1 pharmacological inhibition, MOB1 gene silencing and YAP activation rescued the reduction of YAP activity due to Pontin ...

敲低 Wnt/β-连环蛋白途径的 CYLD 激活可恢复自噬通量并减少 PA 刺激的 NRCM 中 p62 的积累，而 Wnt/β-连环蛋白途径的抑制剂则逆转了这种效应。 因此，我们的研究结果为心肌细胞PA毒性的分子机制提供了新的见解，并表明CYLD可能成为脂毒性心肌病的新治疗靶点。

In this study, we aimed to investigate the role of the Wnt/β-catenin/TCF7L2 signaling and CA2 in the development of DCM. Streptozotocin (STZ)/high-fat diet (HFD)-induced diabetic mice and high glucose-stimulated neonatal rat cardiomyocytes (NRCMs) were used as in-vivo and in-vitro models of Type 2 diabetes (T2DM), respectively.

2017年1月3日 · NRCM or NRCM co-cultured with pre-labelled Control MP 1, Control MP 2, CMMP, and CSC were plated onto fibronectin-coated chamber slides (BD Biosciences) and subsequently fixed with 4% ...

2023年5月9日 · We demonstrate the protective role of PI16 in left ventricular injury and remodeling after MI by suppressing the HDAC1‐Wnt3a (wingless‐type MMTV integration site family, member 3a)‐β‐catenin axis, which means PI16, as an endogenous HDAC1 inhibitor, may provide a promising strategy for MI.

2025年2月16日 · 为了研究出生后哺乳动物心脏中 Pontin 的表达情况，第一作者单位的研究人员分析了野生型（WT）小鼠和大鼠的心脏组织。 蛋白质免疫印迹分析表明，与成年大鼠心脏（12 周龄）相比，新生大鼠心脏（2 - 3 日龄）中 Pontin 的表达显著更高。 在心脏受到压力刺激后，Pontin 的表达也会下降。 在压力超负荷肥大模型中（如之前研究报道，该模型会使心脏重量与胫骨长度的比值增加 1.5 倍），研究人员发现，在进行主动脉弓缩窄（TAC）2 周后，WT 小鼠心脏中 …

2023年6月30日 · 从机械角度来看，itgbl1–nme1–tgf-β–smad2/3 和 wnt 信号通路被确定分别介导 nrcf 激活和 nrcm 肥大。 最后，在 TAC 小鼠中敲低 ITBBL1 重现了体外研究结果，表明心脏纤维化、肥大减弱并改善了心脏功能。

MKK4-inactivated NRCMs, but not WT NRCMs showed increased TGF-b 1 mRNA expression ( Figure 9 A) under basal conditions. In contrast, Col1a1 and MMP2 expression was not significantly different...

2016年6月14日 · Furthermore, overexpression and knockdown of Tcf7l2 in cultured neonatal rat cardiomyocytes (NRCMs) positively and negatively control c-Myc expression and cardiomyocyte hypertrophy, respectively. These results indicate that Wnt/β-catenin signaling is activated in heart failure and can directly regulate target gene expression.