Evidence map›Paper›PMID 30034392›Full record

ArticleFrontiers in immunology2018

Attenuation of Rheumatoid Inflammation by Sodium Butyrate Through Reciprocal Targeting of HDAC2 in Osteoclasts and HDAC8 in T Cells.

Da Som Kim, Jeong-Eun Kwon, Seung Hoon Lee, Eun Kyung Kim, Jun-Geol Ryu, Kyung-Ah Jung, Jeong-Won Choi, Min-Jung Park, Young-Mee Moon, Sung-Hwan Park and 2 more

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

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

67 citing papers in PubMed, 105 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Da Som KimThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Jeong-Eun KwonThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Seung Hoon LeeThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Eun Kyung KimThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Jun-Geol RyuThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Kyung-Ah JungImpact Biotech, Seoul, South Korea.
Jeong-Won ChoiThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Min-Jung ParkThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Young-Mee MoonThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Sung-Hwan ParkDivision of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Mi-La ChoThe Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Seung-Ki KwokDivision of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Catholic University of Korea · KRHarvard University · USSeoul St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease caused by both genetic and environmental factors. Recently, investigators have focused on the gut microbiota, which is thought to be an environmental factor that affects the development of RA. Metabolites secreted by the gut microbiota maintain homeostasis in the gut through various mechanisms [e.g., butyrate, which is one of the major metabolites of gut microbiota, exerts an anti-inflammatory effect by activating G-protein-coupled receptors and inhibiting histone deacetylases (HDACs)]. Here, we focused on the inhibition of the HDACs by butyrate in RA. To this end, we evaluated the therapeutic effects of butyrate in an animal model of autoimmune arthritis. The arthritis score and incidence were lower in the butyrate-treated group compared to the control group. Also, butyrate inhibited HDAC2 in osteoclasts and HDAC8 in T cells, leading to the acetylation of glucocorticoid receptors and estrogen-related receptors α, respectively. Additionally, control of the T

Indexed as

ERRαglucocorticoid receptorhistone deacetylasesrheumatoid arthritissodium butyrate

Identifiers

PMID30034392
PMCPMC6043689
OpenAlexW2872700363

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.