Evidence map›Paper›PMID 42021879›Full record

ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2026

[ROMO1 Promotes the Repair of Radiation-induced Skin Injury by Regulating Mitochondrial Function and Keratinocyte Proliferation].

Tingyi Yang, Wenling Tu, Xiaoyou Tang, Mengjie DU, Adili Maheliya, Zuxiang Yu, Shuai Qu, Hao Bai, Shuyu Zhang

Abstract readEnglish Abstract
In one paragraph

Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 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

9 authors.

Tingyi Yang( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.ORCID 0000-0003-3112-4383
Wenling Tu( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Xiaoyou Tang( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Mengjie DU( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Adili Maheliya( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Zuxiang Yu( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Shuai Qu( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Hao Bai( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Shuyu Zhang( 610041)Laboratory of Radiation Medicine, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.ORCID 0000-0003-1419-3635

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the molecular mechanisms of early mitochondrial stress in keratinocytes induced by ionizing radiation (IR), focusing on the key role of ROMO1 in radiation-induced skin injury (RISI). Methods: HaCaT keratinocytes were used to assess cellular status, mitochondrial dysfunction and oxidative stress at various time points after different irradiation doses. Mitochondrial proteomics at 24 hours post-20 Gy irradiation identified ROMO1 as the protein with the greatest reduction in expression. Results: At 24 hours post-20 Gy irradiation, HaCaT cells exhibited inhibited proliferation ( Conclusion: The mitochondrial protein ROMO1 is a key regulator of the early keratinocyte stress response to radiation. It impedes the repair of radiation-induced skin injury by suppressing cell proliferation via modulation of mitochondrial function. Targeted inhibition of ROMO1 may represent a novel therapeutic strategy to promote healing and prevent chronic progression of radiation-induced skin injury.

Indexed as

Cell ProliferationKeratinocytesMembrane ProteinsMitochondriaMitochondrial ProteinsSkinAnimalsHumansMembrane Potential, MitochondrialMiceMice, KnockoutOxidative StressMembrane ProteinsMitochondrial ProteinsROMO1 protein, humanKeratinocyte proliferationMitochondrial stress responseRadiation-induced skin injuryROMO1

Identifiers

PMID42021879
PMCPMC13095722

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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.