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<p>Overactive lytic regulated cell death (RCD) causes excessive inflammation and impairs tissue repair. Current strategies rely on small-molecule inhibitors targeting the initiation of lytic RCD but these show off-target effects and reduced pro-repair factor release. During lytic RCD, a transitional agonal stage exists between initiation and terminal death, during which cells either proceed to terminal death or undergo resuscitation. Here, we found that agonal cells actively upregulated uptake of extracellular vesicles (EVs), and internalised EVs fused with the plasma membrane via SNARE complexes to enhance membrane repair. We demonstrated that enhancing the membrane repair capacity of agonal cells through artificially prepared EV-mimetic&#xa0;nano-platelet vesicles (NPVs) effectively promoted their resuscitation. Moreover, resuscitated cells secreted substantial amounts of prostaglandin E2 and N1-Acetylspermidine to further promote tissue repair. Our therapeutic strategy for lytic RCD-related delayed tissue repair is based on EV-mediated membrane repair and aims to establish a pro-regenerative niche using NPVs that can drive agonal cell resuscitation.</p>

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Agonal cell resuscitation strategy to promote tissue repair

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月11日

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  • Zhenxiang Huang,
  • Qingqing Wang,
  • Yiyu Chen,
  • Jiahao Zhu,
  • Jiachen Xu,
  • Yang Yang,
  • Yongcheng Wang,
  • Ke Yang,
  • Huige Yan,
  • Mobai Li,
  • Anlan Yang,
  • Liqing Shangguan,
  • Chenhui Gu,
  • Shunwu Fan,
  • Pengfei Chen,
  • Xianfeng Lin

摘要

Overactive lytic regulated cell death (RCD) causes excessive inflammation and impairs tissue repair. Current strategies rely on small-molecule inhibitors targeting the initiation of lytic RCD but these show off-target effects and reduced pro-repair factor release. During lytic RCD, a transitional agonal stage exists between initiation and terminal death, during which cells either proceed to terminal death or undergo resuscitation. Here, we found that agonal cells actively upregulated uptake of extracellular vesicles (EVs), and internalised EVs fused with the plasma membrane via SNARE complexes to enhance membrane repair. We demonstrated that enhancing the membrane repair capacity of agonal cells through artificially prepared EV-mimetic nano-platelet vesicles (NPVs) effectively promoted their resuscitation. Moreover, resuscitated cells secreted substantial amounts of prostaglandin E2 and N1-Acetylspermidine to further promote tissue repair. Our therapeutic strategy for lytic RCD-related delayed tissue repair is based on EV-mediated membrane repair and aims to establish a pro-regenerative niche using NPVs that can drive agonal cell resuscitation.