研究人员首先建立了可诱导的小鼠模型，发现了FH的缺失能够引起明显的代谢变化，包括延胡索酸等代谢标志物的增加，以及干扰素刺激基因、促炎细胞因子、趋化因子的增加等炎症和先天免疫反应相关的通路改变。研究发现了肾脏FH的缺失触发了细胞自主的先天免疫反应，从而导致体内和体外干扰素刺激基因（ISG）的上调。进一步的研究表明，FH的缺失可诱导线粒体DNA（mtDNA）慢性释放到细胞质中，引发持续的炎症反应激活。

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