Evidence map›Paper›PMID 32188057›Full record

ArticleCells2020

SIRT1 Alleviates LPS-Induced IL-1β Production by Suppressing NLRP3 Inflammasome Activation and ROS Production in Trophoblasts.

Sumi Park, Jiha Shin, Jeongyun Bae, Daewon Han, Seok-Rae Park, Jongdae Shin, Sung Ki Lee, Hwan-Woo Park

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Resveratrol Activates SIRT1 to Inhibit Trophoblast Pyroptosis in Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
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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

8 authors at 1 institution in 1 country.

Sumi ParkDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.
Jiha ShinDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.
Jeongyun BaeDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.
Daewon HanDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.
Seok-Rae ParkMyunggok Medical Research Institute, Konyang University College of Medicine, Daejeon 35365, Korea.
Jongdae ShinDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.
Sung Ki LeeMyunggok Medical Research Institute, Konyang University College of Medicine, Daejeon 35365, Korea.
Hwan-Woo ParkDepartment of Cell Biology, Konyang University College of Medicine, Daejeon 35365, Korea.ORCID 0000-0001-8029-2004
Konyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence indicates that aberrant maternal inflammation is associated with several pregnancy-related disorders such as preeclampsia, preterm birth, and intrauterine growth restriction. Sirtuin1 (SIRT1), a class III histone deacetylase, is involved in the regulation of various physiopathological processes including cellular inflammation and metabolism. However, the effect of SIRT1 on the placental proinflammatory environment remains to be elucidated. In this study, we investigated the effect of SIRT1 on lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation and its underlying mechanisms in human first-trimester trophoblasts (Sw.71 and HTR-8/SVneo cells). Treatment with LPS elevated SIRT1 expression and induced NLRP3 inflammasome activation in mouse placental tissues and human trophoblasts. Knockdown of SIRT1 enhanced LPS-induced NLRP3 inflammasome activation, inflammatory signaling, and subsequent interleukin (IL)-1β secretion. Furthermore, knockdown of NLRP3 considerably attenuated the increase of IL-1β secretion in SIRT1-knockdown cells treated with LPS. Moreover, SIRT1 inhibited LPS-induced NLRP3 inflammasome activation by reducing oxidative stress. This study revealed a novel mechanism via which SIRT1 exerts anti-inflammatory effects, suggesting that SIRT1 is a potential therapeutic target for the prevention of inflammation-associated pregnancy-related complications.

Indexed as

AnimalsFemaleHumansInflammasomesInterleukin-1betaLipopolysaccharidesMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPremature BirthReactive Oxygen SpeciesSignal TransductionSirtuin 1TrophoblastsIL1B protein, humanIL1B protein, mouseInflammasomesInterleukin-1betaLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNlrp3 protein, mouseReactive Oxygen SpeciesSIRT1 protein, humanSirt1 protein, mouseSirtuin 1human trophoblastsmaternal inflammationNLRP3 inflammasomeoxidative stressplacentaSIRT1

Identifiers

PMID32188057
PMCPMC7140679
OpenAlexW3010826957

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.