Evidence map›Paper›PMID 40214031›Full record

ArticleJournal of cosmetic dermatology2025

ALKBH5 Inhibits YTHDF2-m6A-Mediated Degradation of RCN1 mRNA to Promote Keloid Formation by Activating IRE1α-XBP1-Mediated ER Stress.

Min Shi, Lu Zhang, Fangfang Bi, Zhuo Zhou

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In one paragraph

Article in Journal of cosmetic dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. 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

4 authors.

Min ShiSchool of Medicine, Xi'an Peihua University, Xi'an, Shaanxi, China.
Lu ZhangSchool of Medicine, Xi'an Peihua University, Xi'an, Shaanxi, China.
Fangfang BiSchool of Medicine, Xi'an Peihua University, Xi'an, Shaanxi, China.
Zhuo ZhouDepartment of Obstetrics and Gynecology, Northwest University First Hospital, Xi'an, Shaanxi, China.ORCID https://orcid.org/0009-0001-0978-9699

Funding

Natural Science Basic Research Program of Shaanxi Province 2022JM-558
6 · The paper itself

Abstract

backgroundReticulocalbin 1 (RCN1) was reported to be upregulated in keloid, but its molecular mechanism remains unclear. The aim of this study is to investigate the role of RCN1 in keloid.

methodsThe expression of RCN1 was detected in keloid tissues. Keloid fibroblasts were transfected with RCN1 overexpression vector. Cell viability, collagen production, apoptosis, and cell invasion were measured. Then, the m6A modification level of RCN1 mRNA was detected by methylated RNA immunoprecipitation (MeRIP), and the effect of overexpression of ALKB homolog5 (ALKBH5) on the m6A modification level of RCN1 mRNA was evaluated. Subsequently, the relationship between RCN1 and XBP1 was verified by co-immunoprecipitation (Co-IP) assay. pcDNA-RCN1 and XBP1 shRNA were transfected into keloid fibroblasts to for reversal experiments, and changes in the endoplasmic reticulum (ER) structure of keloid fibroblasts were observed by transmission electron microscopy (TEM). Finally, we established a mouse keloid model and injected mice with the RCN1 shRNA lentiviral vectors to monitor the keloid formation in mice.

resultsRCN1 was highly expressed in keloid tissues and keloid fibroblasts. Overexpression of RCN1 significantly increased keloid fibroblast viability, collagen production, and invasion, but inhibited cell apoptosis. ALKBH5 upregulated RCN1 expression by reducing m6A-YTHDF2-mediated degradation of RCN1 mRNA, and RCN1 knockdown reversed the promoting effect of ALKBH5 overexpression on cell viability collagen production and invasion, and the inhibitory effect of ALKBH5 overexpression on apoptosis in keloid fibroblasts. Moreover, overexpression of RCN1 significantly upregulated the protein levels of XBP1, GRP78, and IRE1α, and promoted ER stress in keloid fibroblasts, but this change was eliminated by sh-XBP1 intervention. In vivo experiments showed that knockdown of RCN1 significantly inhibited keloid formation by alleviating cell apoptosis and ER stress in mice.

conclusionOur data revealed that RCN1 was upregulated by ALKBH5 to promote keloid formation by activating IRE1α-XBP1-mediated ER stress, RCN1 may be a potential biomarker for treatment of keloid.

Indexed as

AlkB Homolog 5, RNA DemethylaseKeloidRNA-Binding ProteinsX-Box Binding Protein 1AnimalsApoptosisCells, CulturedDisease Models, AnimalEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesFemaleFibroblastsHumansMaleMiceALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanHSPA5 protein, humanHspa5 protein, mouseProtein Serine-Threonine KinasesRNA-Binding ProteinsRNA, MessengerX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouseALKBH5fibroblastsIRE1α‐XBP1keloidRCN1

Identifiers

PMID40214031
PMCPMC11987481

What Socratic holds

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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 Socratic graph.