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<p>Heart failure affects approximately 56 million people worldwide with a 5-year mortality rate exceeding 50%, necessitating new therapeutic strategies. Although low-level vagus nerve stimulation shows promise for treating heart failure, existing devices are limited by short battery life, lack of degradability, and insufficient adaptability to disease progression. Here we develop a fully biodegradable triboelectric nanogenerator for self-powered vagus nerve stimulation that prevents and reverses myocardial remodeling through acetylcholine release modulation. In a murine heart failure model, the device generates 9.07 ± 0.43 V open-circuit voltage and 4.19 ± 0.14 μA short-circuit current, enabling stable stimulation for 4 weeks with rapid ultrasound-triggered degradation. We show that device-based vagus nerve stimulation significantly improves cardiac function, attenuates pathological remodeling, and favorably modulates heart failure-related gene expression across multiple disease stages. This technology eliminates battery replacement surgeries and device removal procedures, establishing a paradigm for personalized, stage-specific heart failure therapy.</p>

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A fully degradable triboelectric vagus nerve stimulator for attenuating cardiac remodeling and heart failure at different stages

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月21日

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  • Zhen Guo,
  • Sheng-Yu Chao,
  • Chun-Yan Kong,
  • Ling-Ling Xu,
  • Xi Cui,
  • Yuan Xi,
  • Yi-Chang Quan,
  • Ming-Yu Wang,
  • Yu-Lan Ma,
  • Xiu-Jun Dai,
  • Zhou Li,
  • Qi-Zhu Tang

摘要

Heart failure affects approximately 56 million people worldwide with a 5-year mortality rate exceeding 50%, necessitating new therapeutic strategies. Although low-level vagus nerve stimulation shows promise for treating heart failure, existing devices are limited by short battery life, lack of degradability, and insufficient adaptability to disease progression. Here we develop a fully biodegradable triboelectric nanogenerator for self-powered vagus nerve stimulation that prevents and reverses myocardial remodeling through acetylcholine release modulation. In a murine heart failure model, the device generates 9.07 ± 0.43 V open-circuit voltage and 4.19 ± 0.14 μA short-circuit current, enabling stable stimulation for 4 weeks with rapid ultrasound-triggered degradation. We show that device-based vagus nerve stimulation significantly improves cardiac function, attenuates pathological remodeling, and favorably modulates heart failure-related gene expression across multiple disease stages. This technology eliminates battery replacement surgeries and device removal procedures, establishing a paradigm for personalized, stage-specific heart failure therapy.