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<p>Sepsis-induced multiple organ dysfunction syndrome (MODS) represents one of the most lethal complications in critical care medicine, posing a severe threat to patient survival. The interplay between mitochondrial dysfunction and inflammasome activation has recently emerged as a pivotal mechanism in the pathogenesis of MODS. Mitochondrial damage not only induces oxidative stress, disrupts energy metabolism, and initiates programmed cell death but also activates inflammasomes via the release of damage-associated molecular patterns (DAMPs). This activation triggers a cascade of inflammatory responses, thereby exacerbating organ dysfunction. Aberrant activation of inflammasomes, particularly the NLRP3 inflammasome, has been demonstrated to directly promote the release of multiple proinflammatory cytokines, constituting a critical event in MODS progression. As research on the mitochondria–inflammasome axis deepens, potential therapeutic strategies targeting this axis, including antioxidants, metabolic modulators, and specific inflammasome inhibitors, have shown promising translational potential. This review systematically outlines recent advances in this field, aiming to provide new insights into the molecular mechanisms of sepsis-induced MODS and to inform the development of novel therapeutic interventions.</p>

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The mitochondria–inflammasome axis in sepsis-induced multiple organ dysfunction syndrome: mechanisms and therapeutic advances

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月20日

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  • Xiangxin Liao,
  • Yifei Chen,
  • Yixin Cheng,
  • Boya Gong,
  • Zhaohui Zhang,
  • Xingguang Qu,
  • Gaosheng Zhou

摘要

Sepsis-induced multiple organ dysfunction syndrome (MODS) represents one of the most lethal complications in critical care medicine, posing a severe threat to patient survival. The interplay between mitochondrial dysfunction and inflammasome activation has recently emerged as a pivotal mechanism in the pathogenesis of MODS. Mitochondrial damage not only induces oxidative stress, disrupts energy metabolism, and initiates programmed cell death but also activates inflammasomes via the release of damage-associated molecular patterns (DAMPs). This activation triggers a cascade of inflammatory responses, thereby exacerbating organ dysfunction. Aberrant activation of inflammasomes, particularly the NLRP3 inflammasome, has been demonstrated to directly promote the release of multiple proinflammatory cytokines, constituting a critical event in MODS progression. As research on the mitochondria–inflammasome axis deepens, potential therapeutic strategies targeting this axis, including antioxidants, metabolic modulators, and specific inflammasome inhibitors, have shown promising translational potential. This review systematically outlines recent advances in this field, aiming to provide new insights into the molecular mechanisms of sepsis-induced MODS and to inform the development of novel therapeutic interventions.