Evidence map›Paper›PMID 34858401›Full record

ArticleFrontiers in immunology2021

Targeting TBK1 Attenuates LPS-Induced NLRP3 Inflammasome Activation by Regulating of mTORC1 Pathways in Trophoblasts.

Sohee Lee, Jiha Shin, Jong-Seok Kim, Jongdae Shin, Sung Ki Lee, Hwan-Woo Park

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Innate Immunity and Microbial Recognition in Reproduction: From Barrier Defense to Maternal-Fetal Tolerance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Single-particle rotational microrheology enables pathological staging of macrophage foaming and antiatherosclerotic studies.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Sohee LeeDepartment of Cell Biology, Konyang University College of Medicine, Daejeon, South Korea.
Jiha ShinDepartment of Cell Biology, Konyang University College of Medicine, Daejeon, South Korea.
Jong-Seok KimMyunggok Medical Research Institute, Konyang University College of Medicine, Daejeon, South Korea.
Jongdae ShinDepartment of Cell Biology, Konyang University College of Medicine, Daejeon, South Korea.
Sung Ki LeeMyunggok Medical Research Institute, Konyang University College of Medicine, Daejeon, South Korea.
Hwan-Woo ParkDepartment of Cell Biology, Konyang University College of Medicine, Daejeon, South Korea.
Konyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathological maternal inflammation and abnormal placentation contribute to several pregnancy-related disorders, including preterm birth, intrauterine growth restriction, and preeclampsia. TANK-binding kinase 1 (TBK1), a serine/threonine kinase, has been implicated in the regulation of various physiological processes, including innate immune response, autophagy, and cell growth. However, the relevance of TBK1 in the placental pro-inflammatory environment has not been investigated. In this study, we assessed the effect of TBK1 inhibition on lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation and its underlying mechanisms in human trophoblast cell lines and mouse placenta. TBK1 phosphorylation was upregulated in the trophoblasts and placenta in response to LPS. Pharmacological and genetic inhibition of TBK1 in trophoblasts ameliorated LPS-induced NLRP3 inflammasome activation, placental inflammation, and subsequent interleukin (IL)-1 production. Moreover, maternal administration of amlexanox, a TBK1 inhibitor, reversed LPS-induced adverse pregnancy outcomes. Notably, TBK1 inhibition prevented LPS-induced NLRP3 inflammasome activation by targeting the mammalian target of rapamycin complex 1 (mTORC1). Thus, this study provides evidence for the biological significance of TBK1 in placental inflammation, suggesting that amlexanox may be a potential therapeutic candidate for treating inflammation-associated pregnancy-related complications.

Indexed as

AnimalsFemaleHumansInflammasomesInflammationLipopolysaccharidesMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPlacentaPregnancyPregnancy ComplicationsProtein Serine-Threonine KinasesTrophoblastsInflammasomesLipopolysaccharidesMechanistic Target of Rapamycin Complex 1NLR Family, Pyrin Domain-Containing 3 ProteinProtein Serine-Threonine KinasesTBK1 protein, humanmaternal inflammationmTORC1NLRP3 inflammasomeplacentaTBK1trophoblast

Identifiers

PMID34858401
PMCPMC8630692
OpenAlexW3211435435

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.