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Objective <p>To develop and evaluate a mitochondria-targeted biomimetic nanoplatform (nMitoQ-SNA-CMT) for the treatment of intervertebral disc degeneration (IVDD).</p> Methods <p>A rat IVDD model and an H<sub>2</sub>O<sub>2</sub>-induced oxidative stress model in nucleus pulposus cells (NPCs) were established to investigate the effects of nMitoQ-SNA-CMT on mitochondrial function, oxidative stress, mitophagy, inflammatory signaling, and cellular senescence. Molecular, cellular, and histological analyses were used to evaluate therapeutic efficacy in vitro and in vivo.</p> Results <p>nMitoQ-SNA-CMT efficiently targeted mitochondria, scavenged excessive reactive oxygen species (ROS), and silenced miR-141-3p, thereby activating SESN2-dependent UPRmt and mitophagy. This dual action markedly reduced mitochondrial DNA release and suppressed cGAS–STING pathway activation, leading to attenuation of NPC senescence, inflammatory responses, and extracellular matrix degradation. In IVDD rat models, nMitoQ-SNA-CMT significantly restored disc structure and function and outperformed free MitoQ and non-coated nanoparticles.</p> Conclusion <p>nMitoQ-SNA-CMT represents a potent and safe therapeutic strategy for IVDD by coordinately regulating mitochondrial oxidative stress, mitophagy, and innate immune activation, providing a promising platform for precision nanomedicine in degenerative disc diseases.</p> Graphical abstract <p></p>

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Biomimetic nanoplatforms modulating mitochondrial pathways in IVDD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月2日

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  • Jian-Bin Guan,
  • Shan-Xi Wang,
  • Ying-Guang Wang,
  • Kai-Yuan Lin,
  • Ren-Ji Wang,
  • Rui-Rui Bu,
  • Yuan-Ting Zhao,
  • Si-Bo Wang,
  • Ling-Jiang Li,
  • Xiao-Jun Yu

摘要

Objective

To develop and evaluate a mitochondria-targeted biomimetic nanoplatform (nMitoQ-SNA-CMT) for the treatment of intervertebral disc degeneration (IVDD).

Methods

A rat IVDD model and an H2O2-induced oxidative stress model in nucleus pulposus cells (NPCs) were established to investigate the effects of nMitoQ-SNA-CMT on mitochondrial function, oxidative stress, mitophagy, inflammatory signaling, and cellular senescence. Molecular, cellular, and histological analyses were used to evaluate therapeutic efficacy in vitro and in vivo.

Results

nMitoQ-SNA-CMT efficiently targeted mitochondria, scavenged excessive reactive oxygen species (ROS), and silenced miR-141-3p, thereby activating SESN2-dependent UPRmt and mitophagy. This dual action markedly reduced mitochondrial DNA release and suppressed cGAS–STING pathway activation, leading to attenuation of NPC senescence, inflammatory responses, and extracellular matrix degradation. In IVDD rat models, nMitoQ-SNA-CMT significantly restored disc structure and function and outperformed free MitoQ and non-coated nanoparticles.

Conclusion

nMitoQ-SNA-CMT represents a potent and safe therapeutic strategy for IVDD by coordinately regulating mitochondrial oxidative stress, mitophagy, and innate immune activation, providing a promising platform for precision nanomedicine in degenerative disc diseases.

Graphical abstract