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<p>Female reproductive disorders, including endometriosis, polycystic ovary syndrome (PCOS), preeclampsia (PE), recurrent pregnancy loss (RPL), premature ovarian insufficiency (POI), and implantation-related complications, are frequently associated with chronic inflammation, immune dysregulation, and impaired tissue homeostasis. Increasing evidence suggests that inflammasomes play central roles in regulating inflammatory responses and multiple forms of programmed cell death, including apoptosis, pyroptosis, necroptosis, and the recently described integrated cell death pathway known as PANoptosis. Inflammasome activation promotes the maturation of pro-inflammatory cytokines such as interleukin (IL)-1β and IL-18 and contributes to cellular and tissue injury through downstream cell death signaling pathways. Here, we review the existing knowledge on the molecular mechanisms linking inflammasome signaling to the regulated cell death pathways in female reproductive disorders. The role of apoptosis, pyroptosis and necroptosis in the pathogenesis of endometriosis, PCOS, PE, RPL, POI and other pregnancy related complications and the role of NLRP3 and other inflammasome complexes in disease progression are discussed. Recent studies suggest that crosstalk between these cell death pathways can lead to inflammatory pathology via PANoptosis-related mechanisms, although direct evidence for PANoptosis in reproductive diseases is still lacking. We also review current and potential therapeutic approaches targeting inflammasomes and associated cell death pathways such as NLRP3 inhibitors, IL-1β blockade and regulators of pyroptotic signaling. Together, the available evidence suggest that inflammasome-associated cell death pathways are important contributors to reproductive disease pathogenesis and may offer new diagnostic and therapeutic opportunities. Further mechanistic and clinical studies are needed to elucidate the role of PANoptosis and determine whether targeting key inflammasome and PANoptosis-related regulators can improve reproductive outcomes.</p> Graphical abstract <p></p>

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Inflammasome-mediated cell death pathways in female reproductive disorders: from apoptosis, pyroptosis, and necroptosis to PANoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月29日

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  • Amirhossein Mardi,
  • Hamid Ahmadi,
  • Samaneh Abdolmohammadi-Vahid,
  • Pouya Zahmatkesh,
  • Golaleh Savari,
  • Mohammad Sadegh Soltani-Zangbar,
  • Leili Aghebati-Maleki

摘要

Female reproductive disorders, including endometriosis, polycystic ovary syndrome (PCOS), preeclampsia (PE), recurrent pregnancy loss (RPL), premature ovarian insufficiency (POI), and implantation-related complications, are frequently associated with chronic inflammation, immune dysregulation, and impaired tissue homeostasis. Increasing evidence suggests that inflammasomes play central roles in regulating inflammatory responses and multiple forms of programmed cell death, including apoptosis, pyroptosis, necroptosis, and the recently described integrated cell death pathway known as PANoptosis. Inflammasome activation promotes the maturation of pro-inflammatory cytokines such as interleukin (IL)-1β and IL-18 and contributes to cellular and tissue injury through downstream cell death signaling pathways. Here, we review the existing knowledge on the molecular mechanisms linking inflammasome signaling to the regulated cell death pathways in female reproductive disorders. The role of apoptosis, pyroptosis and necroptosis in the pathogenesis of endometriosis, PCOS, PE, RPL, POI and other pregnancy related complications and the role of NLRP3 and other inflammasome complexes in disease progression are discussed. Recent studies suggest that crosstalk between these cell death pathways can lead to inflammatory pathology via PANoptosis-related mechanisms, although direct evidence for PANoptosis in reproductive diseases is still lacking. We also review current and potential therapeutic approaches targeting inflammasomes and associated cell death pathways such as NLRP3 inhibitors, IL-1β blockade and regulators of pyroptotic signaling. Together, the available evidence suggest that inflammasome-associated cell death pathways are important contributors to reproductive disease pathogenesis and may offer new diagnostic and therapeutic opportunities. Further mechanistic and clinical studies are needed to elucidate the role of PANoptosis and determine whether targeting key inflammasome and PANoptosis-related regulators can improve reproductive outcomes.

Graphical abstract