Evidence map›Paper›PMID 28966618›Full record

ArticleFrontiers in immunology2017

SIRT1/Adenosine Monophosphate-Activated Protein Kinase α Signaling Enhances Macrophage Polarization to an Anti-inflammatory Phenotype in Rheumatoid Arthritis.

So Youn Park, Sung Won Lee, Sang Yeob Lee, Ki Whan Hong, Sun Sik Bae, Koanhoi Kim, Chi Dae Kim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Article
  3. Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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  10. Effect of Estrogen on Sirt1 Signaling in Human Macrophages.International journal of molecular sciences · 2025
    Article
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  14. Regulatory Roles for SIRT1 in Aging and Immunosenescence.Results and problems in cell differentiation · 2025
    Review
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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

7 authors at 2 institutions in 1 country.

So Youn ParkDepartment of Pharmacology, School of Medicine, Pusan National University, Gyeongsangnam-do, South Korea.
Sung Won LeeDepartment of Internal Medicine, College of Medicine, Dong-A University, Busan, South Korea.
Sang Yeob LeeDepartment of Internal Medicine, College of Medicine, Dong-A University, Busan, South Korea.
Ki Whan HongGene and Cell Therapy Research Center for Vessel-Associated Diseases, Pusan National University, Gyeongsangnam-do, South Korea.
Sun Sik BaeDepartment of Pharmacology, School of Medicine, Pusan National University, Gyeongsangnam-do, South Korea.
Koanhoi KimDepartment of Pharmacology, School of Medicine, Pusan National University, Gyeongsangnam-do, South Korea.
Chi Dae KimDepartment of Pharmacology, School of Medicine, Pusan National University, Gyeongsangnam-do, South Korea.
Pusan National University · KRDong-A University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are crucially involved in the pathogenesis of rheumatoid arthritis (RA). Macrophages of the M1 phenotype act as pro-inflammatory mediators in synovium, whereas those of the M2 phenotype suppress inflammation and promote tissue repair. SIRT1 is a class 3 histone deacetylase with anti-inflammatory characteristics. However, the role played by SIRT1 in macrophage polarization has not been defined in RA. We investigated whether SIRT1 exerts anti-inflammatory effects by modulating M1/M2 polarization in macrophages from RA patients. In this study, SIRT1 activation promoted the phosphorylation of an adenosine monophosphate-activated protein kinase (AMPK) α/acetyl-CoA carboxylase in macrophages exposed to interleukin (IL)-4, and that this resulted in the expressions of M2 genes, including MDC, FcεRII, MrC1, and IL-10, at high levels. Furthermore, these expressions were inhibited by sirtinol (an inhibitor of SIRT1) and compound C (an inhibitor of AMPK). Moreover, SIRT1 activation downregulated LPS/interferon γ-mediated NF-κB activity by inhibiting p65 acetylation and the expression of M1 genes, such as CCL2, iNOS, IL-12 p35, and IL-12 p40. Macrophages from SIRT1 transgenic (Tg)-mice exhibited enhanced polarization of M2 phenotype macrophages and reduced polarization of M1 phenotype macrophages. In line with these observations, SIRT1-Tg mice showed less histological signs of arthritis, that is, lower TNFα and IL-1β expressions and less severe arthritis in the knee joints, compared to wild-type mice. Taken together, the study shows activation of SIRT1/AMPKα signaling exerts anti-inflammatory activities by regulating M1/M2 polarization, and thereby reduces inflammatory responses in RA. Furthermore, it suggests that SIRT1 signaling be viewed as a therapeutic target in RA.

Indexed as

adenosine monophosphate-activated protein kinase αinflammationM1/M2 macrophagesmacrophage polarizationrheumatoid arthritisSIRT1

Identifiers

PMID28966618
PMCPMC5605563
OpenAlexW2756093409

What OpenQuestion holds

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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.