A new role of the early endosome in restricting NLRP3 inflammasome via mitophagy

King Yip Cheng, Ka Lok Wu

Research output: Journal article publicationJournal articleAcademic researchpeer-review

3 Citations (Scopus)


NLRP3 (NLR family pyrin domain containing 3) inflammasome is a potent mediator of inflammation due to its ability to produce the pro-inflammatory cytokines IL1B (interleukin 1 beta) and IL18 in response to numerous danger signals and pathogens. Mitophagy, a selective form of autophagy, restricts NLRP3 inflammasome activation by limiting the mitochondrial-derived danger signals. Here, we demonstrated that the adaptor protein APPL1 together with its interaction partner RAB5 in early endosomes negatively regulate NLRP3 inflammasome activation via induction of mitophagy in macrophages. Hematopoietic-deletion of Appl1 exacerbates systemic NLRP3 inflammasome activation in rodent models under obese or septic conditions. Our study identified a new regulatory network between early endosomes and mitochondria in control of NLRP3 inflammasome activation.

Original languageEnglish
Pages (from-to)1475-1477
Number of pages3
Issue number6
Publication statusPublished - 25 Feb 2022


  • APPL1
  • NLRP3 inflammasome
  • RAB5
  • early endosome
  • mitochondria
  • mitophagy

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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