Evidence map›Paper›PMID 40201180›Full record

ArticleFrontiers in immunology2025

Curcumin targets YAP1 to enhance mitochondrial function and autophagy, protecting against UVB-induced photodamage.

Quan Chen, Wenxin Lin, Yi Tang, Fengmei He, Bihua Liang, Jiaoquan Chen, Huaping Li, Huilan Zhu

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
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  3. Inhibition of PI3K/Akt/mTOR signaling by curcumin: a novel approach to mitigate synovial fibrosis in knee osteoarthritis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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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.

Quan ChenDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Wenxin LinDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Yi TangDepartment of Dermatology, Guangzhou First People's Hospital, Guangzhou, Guangdong, China.
Fengmei HeDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Bihua LiangDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Jiaoquan ChenDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Huaping LiDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
Huilan ZhuDepartment of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Ultraviolet B (UVB) radiation is a major environmental factor contributing to skin damage via DNA damage, oxidative stress, inflammation, and collagen degradation. It penetrates the epidermis, disrupts DNA integrity, and generates reactive oxygen species (ROS), activating pro-inflammatory pathways such as NF-κB and AP-1, and inducing matrix metalloproteinases (MMPs). These processes lead to structural skin changes, inflammation, and pigmentation disorders like melasma. Cumulative DNA damage from UVB also drives photocarcinogenesis, with nearly 90% of melanomas associated with UV radiation (UVR). Despite clinical interventions like phototherapy and antioxidants, effective treatments for UVB-induced damage remain limited due to side effects and efficacy issues. Methods: This study investigates the protective effects of curcumin on UVB-induced skin damage using a mouse UVB irradiation model and HaCaT cells exposed to UVB Results: Curcumin significantly alleviated UVB-induced skin lesions and inflammation Conclusion: Curcumin treatment markedly improved UVB-induced skin lesions and reduced epidermal inflammation and thickness

Indexed as

AutophagyCurcuminMitochondriaSkinTranscription FactorsUltraviolet RaysAnimalsApoptosisHaCaT CellsHumansMiceReactive Oxygen SpeciesYAP-Signaling ProteinsCurcuminReactive Oxygen SpeciesTranscription FactorsYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteinsautophagycurcuminmitochondrialphotoprotectionskin damageUVBYAP1

Identifiers

PMID40201180
PMCPMC11975583

What OpenQuestion holds

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LicenceCC BY
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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.