Evidence map›Paper›PMID 42609463›Full record

ArticleFrontiers in immunology2026

Inhibition of fatty acid-binding protein 4 alleviates psoriasis-like skin inflammation by modulating macrophage polarization.

Bo Mi Kang, Hyun Seung Choi, Bo Ri Kim, Sang Woong Youn, Hyun Jung Kwon, Jin-Ku Lee, Christine Suh-Yun Joh, Hyo Jeong Nam, Soyoung Jeong, Hyun Woo Kim and 4 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Bo Mi Kang *Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Hyun Seung Choi *Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Bo Ri KimDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Sang Woong YounDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Hyun Jung KwonDepartment of Pathology, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Jin-Ku LeeDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.
Christine Suh-Yun JohDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Hyo Jeong NamDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Soyoung JeongDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Hyun Woo KimDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Jeong Eun KimDepartment of Dermatology, Hanyang University College of Medicine, Seoul, Republic of Korea.
Tae-Gyun KimDepartment of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyun Je KimDepartment of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.
Chong Won ChoiDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatty acid-binding proteins (FABPs) are intracellular lipid chaperones that regulate gene expression by controlling lipid trafficking within subcellular organelles. Among them, FABP4 is primarily expressed in adipocytes and macrophages and has been implicated in inflammatory responses in adipose tissue; however, its role in skin inflammation remains poorly understood. Here, we investigated the immunomodulatory role of FABP4 using human psoriatic skin samples, single-cell RNA sequencing, and an imiquimod-induced mouse model of psoriasis. We further employed pharmacologic inhibition and genetic modulation of FABP4 to assess its effects on macrophage polarization, along with transcription factor regulon analyses to identify downstream regulatory mechanisms. FABP4 was highly expressed in macrophages infiltrating psoriatic skin, and

Indexed as

Fatty Acid-Binding ProteinsMacrophage ActivationMacrophagesPsoriasisSkinAnimalsDisease Models, AnimalFemaleHumansImiquimodMaleMiceMice, Inbred C57BLPPAR gammaFABP4 protein, humanFatty Acid-Binding ProteinsImiquimodPPAR gammafatty acid-binding protein 4macrophagemacrophage polarizationPPARGpsoriasis

Identifiers

PMID42609463
PMCPMC13478135

What OpenQuestion holds

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Registered trials

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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.