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<p>Cardiac hypertrophy is one of the significant causes of heart failure and is closely related to the rising rate of hospitalization and readmissions. Given the diverse regulatory roles of alternative splicing in cardiovascular diseases, RNA-binding proteins have attracted increasing research attention. Here, for the first time, we discovered elevated expression of RBMS1 in heart tissues of patients with dilated cardiomyopathy and in mice with cardiac hypertrophy. We demonstrated that RBMS1 activated the PI3K/AKT signaling pathway by promoting the splicing CTTN to generate CTTN-Δe11 splicing isoform, resulting in cytoskeleton and sarcomere damage in cardiomyocytes. Additionally, pharmacological inhibition of RBMS1 by nortriptyline alleviated cardiac hypertrophy and heart failure. These results provide a new perspective for developing novel therapeutic approaches for cardiac hypertrophy and establish a theoretical basis for targeting RBMS1 in the clinical treatment of cardiac hypertrophy.</p>

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RBMS1 orchestrates cardiac hypertrophy by facilitating CTTN splice-switching and sarcomere dynamics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月10日

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  • Liangliang Li,
  • Tianyu Li,
  • Bin Wang,
  • Jiayue Feng,
  • Nan Zhang,
  • Jing Zhang,
  • Zhihui Niu,
  • Wei Li,
  • Huiying Gao,
  • Qianqian Wang,
  • Yang Liu,
  • Yi Chen,
  • Yixin Zhang,
  • Yu Bian,
  • Tengfei Pan,
  • Siqi Sheng,
  • Xuelian Li,
  • Jinping Liu,
  • Baofeng Yang,
  • Haihai Liang

摘要

Cardiac hypertrophy is one of the significant causes of heart failure and is closely related to the rising rate of hospitalization and readmissions. Given the diverse regulatory roles of alternative splicing in cardiovascular diseases, RNA-binding proteins have attracted increasing research attention. Here, for the first time, we discovered elevated expression of RBMS1 in heart tissues of patients with dilated cardiomyopathy and in mice with cardiac hypertrophy. We demonstrated that RBMS1 activated the PI3K/AKT signaling pathway by promoting the splicing CTTN to generate CTTN-Δe11 splicing isoform, resulting in cytoskeleton and sarcomere damage in cardiomyocytes. Additionally, pharmacological inhibition of RBMS1 by nortriptyline alleviated cardiac hypertrophy and heart failure. These results provide a new perspective for developing novel therapeutic approaches for cardiac hypertrophy and establish a theoretical basis for targeting RBMS1 in the clinical treatment of cardiac hypertrophy.