Evidence map›Paper›PMID 37076497›Full record

ArticleCell death & disease2023

LncRNA UCA1 promotes keratinocyte-driven inflammation via suppressing METTL14 and activating the HIF-1α/NF-κB axis in psoriasis.

Yibo Hu, Li Lei, Ling Jiang, Hongliang Zeng, Yushan Zhang, Chuhan Fu, Haoran Guo, Yumeng Dong, Yujie Ouyang, Xiaolin Zhang and 3 more

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

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.3field-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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. RNA mActa pharmacologica Sinica · 2026
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  17. The Role of MClinical reviews in allergy & immunology · 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

13 authors at 2 institutions in 1 country.

Yibo Hu *Department of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Li Lei *Department of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Ling JiangDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Hongliang ZengCenter of Medical Laboratory Animal, Hunan Academy of Chinese Medicine, No.128 Yuehua Road, Changsha, Hunan, 410013, PR China.
Yushan ZhangDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Chuhan FuDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Haoran GuoDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Yumeng DongDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Yujie OuyangDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Xiaolin ZhangDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Jinhua HuangDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China.
Qinghai ZengDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China. zengqinghai@csu.edu.cn.ORCID 0000-0002-6747-1486
Jing ChenDepartment of Dermatology, the Third Xiangya Hospital, Central South University, No.138 Tongzipo Road, Changsha, Hunan, 410013, PR China. 43700351@qq.com.ORCID 0000-0002-7612-4777
Central South University · CNHunan Academy of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keratinocytes are closely associated with innate immunity and inflammatory responses, and are dysregulated during the development of psoriasis, but the underlying mechanisms are not yet fully understood. This work aims to reveal the effects of long non-coding RNA (lncRNA) UCA1 in psoriatic keratinocytes. UCA1 was identified as a psoriasis-related lncRNA that highly expressed in psoriatic lesions. The transcriptome and proteome data of keratinocyte cell line HaCaT showed that UCA1 could positively regulate inflammatory functions, such as response to cytokine. Furthermore, UCA1 silencing decreased inflammatory cytokine secretion and innate immunity gene expression in HaCaT, its culture supernatant also decreased the migration and tube formation ability of vascular endothelial cells (HUVECs). Mechanistically, UCA1 activated the NF-κB signaling pathway, which is regulated by HIF-1α and STAT3. We also observed a direct interaction between UCA1 and N6-methyladenosine (m

Indexed as

PsoriasisRNA, Long NoncodingCell ProliferationCytokinesEndothelial CellsHumansInflammationKeratinocytesMethyltransferasesNF-kappa BCytokinesMethyltransferasesMETTL14 protein, humanNF-kappa BRNA, Long Noncoding

Identifiers

PMID37076497
PMCPMC10115875
OpenAlexW4366583105

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.