PDF(Pubmed)
Abstract：
Endometriosis, affecting 6%-10% of women, often leads to pain and infertility and its underlying inflammatory mechanisms are poorly understood. We established endometriosis models in wild-type and IL16KO mice, revealing the driver function of IL-16 in initiating endometriosis-related inflammation. Using an in vitro system, we confirmed iron overload-induced GSDME-mediated pyroptosis as a key trigger for IL-16 activation and release. In addition, our research led to the development of Z30702029, a compound inhibiting GSDME-NTD-mediated pyroptosis, which shows promise as a therapeutic intervention for endometriosis. Importantly, our findings extend beyond endometriosis, highlighting GSDME-mediated pyroptosis as a broader pathway for IL-16 release and offering insights into potential treatments for various inflammatory conditions.
摘要：
子宫内膜异位症,影响6%-10%的女性，通常会导致疼痛和不育，其潜在的炎症机制知之甚少。我们在野生型和IL16KO小鼠中建立了子宫内膜异位症模型，揭示IL-16在引发子宫内膜异位症相关炎症中的驱动功能。使用体外系统，我们证实铁过载诱导的GSDME介导的焦凋亡是IL-16激活和释放的关键触发因素.此外,我们的研究导致了Z30702029的开发，这是一种抑制GSDME-NTD介导的焦亡的化合物，这表明有望作为子宫内膜异位症的治疗干预。重要的是,我们的发现超越了子宫内膜异位症,强调GSDME介导的焦亡是IL-16释放的更广泛途径，并提供各种炎症条件的潜在治疗方法。
