Evidence map›Paper›PMID 38533495›Full record

ArticleFrontiers in immunology2024

Imidazole propionate ameliorates atopic dermatitis-like skin lesions by inhibiting mitochondrial ROS and mTORC2.

Ha Eun Kim, Jong Yeong Lee, Dong-Hoon Yoo, Hyo-Hyun Park, Eun-Ju Choi, Kyung-Hwa Nam, Jin Park, Jin Kyeong Choi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
7.5field-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

14 citing papers in PubMed, 14 citations in OpenAlex.

  1. The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  8. International journal of molecular sciences · 2025
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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 4 institutions in 1 country.

Ha Eun Kim *Department of Immunology, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Jong Yeong Lee *Department of Immunology, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Dong-Hoon YooDepartment of Sports Rehabilitation and Exercise Management, University of Gyeongnam Geochang, Geochang-gun, Republic of Korea.
Hyo-Hyun ParkDepartment of Clinical Pathology, Daegu Health College, Daegu, Republic of Korea.
Eun-Ju ChoiDepartment of Physical Education, College of Education, Daegu Catholic University, Gyeongsan, Republic of Korea.
Kyung-Hwa NamDepartment of Dermatology, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Jin ParkDepartment of Dermatology, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Jin Kyeong ChoiDepartment of Immunology, Jeonbuk National University Medical School, Jeonju, Republic of Korea.
Jeonbuk National University · KRDaegu Catholic University · KRDaegu Health College · KRGyeongnam Provincial Geochang College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Imidazole propionate (IMP) is a histidine metabolite produced by some gut microorganisms in the human colon. Increased levels of IMP are associated with intestinal inflammation and the development and progression of cardiovascular disease and diabetes. However, the anti-inflammatory activity of IMP has not been investigated. This study aimed to elucidate the role of IMP in treating atopic dermatitis (AD). Methods: To understand how IMP mediates immunosuppression in AD, IMP was intraperitoneally injected into a Results: Contrary to the prevailing view that IMP is an unhealthy microbial metabolite, we found that IMP-treated AD-like skin lesions mice showed significant improvement in their clinical symptoms, including ear thickness, epidermal and dermal thickness, and IgE levels. Furthermore, IMP antagonized the expansion of myeloid (neutrophils, macrophages, eosinophils, and mast cells) and Th cells (Th1, Th2, and Th17) in mouse skin and prevented mitochondrial reactive oxygen species production by inhibiting mitochondrial energy production. Interestingly, we found that IMP inhibited AD by reducing glucose uptake in cells to suppress proinflammatory cytokines and chemokines in an AD-like Discussion: Our results suggest that IMP exerts anti-inflammatory effects through the metabolic reprogramming of skin inflammation, making it a promising therapeutic candidate for AD and related skin diseases.

Indexed as

Dermatitis, AtopicImidazolesAnimalsAnti-Inflammatory AgentsHumansImmunoglobulin EInflammationMiceReactive Oxygen SpeciesSkin5-imidazolepropionic acidAnti-Inflammatory AgentsImidazolesImmunoglobulin EReactive Oxygen SpeciesAMPKatopic dermatitisDDIT4imidazole propionatemitochondria ROSmTORC2

Identifiers

PMID38533495
PMCPMC10964488
OpenAlexW4392715739

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.