Evidence map›Paper›PMID 37359517›Full record

ArticleFrontiers in immunology2023

Apilimod activates the NLRP3 inflammasome through lysosome-mediated mitochondrial damage.

Yingting Hou, Hongbin He, Ming Ma, Rongbin Zhou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Development of a Second-Generation,Journal of medicinal chemistry · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Progress in the Correlation Between Inflammasome NLRP3 and Liver Fibrosis.Journal of clinical and translational hepatology · 2024
    Review
  17. Lysosomal TRPML1 triggers global CaFrontiers in physiology · 2024
    Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Yingting HouCenter for Advanced Interdisciplinary Science and Biomedicine of Institute of Health and Medicine (IHM), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Hongbin HeCenter for Advanced Interdisciplinary Science and Biomedicine of Institute of Health and Medicine (IHM), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Ming MaCenter for Advanced Interdisciplinary Science and Biomedicine of Institute of Health and Medicine (IHM), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Rongbin ZhouCenter for Advanced Interdisciplinary Science and Biomedicine of Institute of Health and Medicine (IHM), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Chinese Academy of Sciences · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NLRP3 is an important innate immune sensor that responses to various signals and forms the inflammasome complex, leading to IL-1β secretion and pyroptosis. Lysosomal damage has been implicated in NLRP3 inflammasome activation in response to crystals or particulates, but the mechanism remains unclear. We developed the small molecule library screening and found that apilimod, a lysosomal disruptor, is a selective and potent NLRP3 agonist. Apilimod promotes the NLRP3 inflammasome activation, IL-1β secretion, and pyroptosis. Mechanismically, while the activation of NLRP3 by apilimod is independent of potassium efflux and directly binding, apilimod triggers mitochondrial damage and lysosomal dysfunction. Furthermore, we found that apilimod induces TRPML1-dependent calcium flux in lysosomes, leading to mitochondrial damage and the NLRP3 inflammasome activation. Thus, our results revealed the pro-inflammasome activity of apilimod and the mechanism of calcium-dependent lysosome-mediated NLRP3 inflammasome activation.

Indexed as

InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinCalciumCarrier ProteinsHydrazonesLysosomesMorpholinesPyrimidinesapilimodCalciumCarrier ProteinsHydrazonesInflammasomesMorpholinesNLR Family, Pyrin Domain-Containing 3 ProteinPyrimidinesactivationapilimodlysosomemitochondriaNLRP3 inflammasome

Identifiers

PMID37359517
PMCPMC10285205
OpenAlexW4380051624

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.