Evidence map›Paper›PMID 41087666›Full record

ArticleCommunications biology2025

LAPTM5 exacerbates STING-mediated inflammation induced by LL-37 through stabilizing STING in rosacea.

Wenyue Huang, Hailun He, Haien Wu, Yichong Wang, Jingyu Wang, Yan Sun, Hexiao Wang, Shulan Yao, Linlin Zhu, Yi Jiang and 2 more

Abstract read
In one paragraph

Article in Communications biology, 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. Article
  2. Article
  3. Article
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

12 authors.

Wenyue HuangDepartment of Dermatology, Shengjing Hospital of China Medical University, Shenyang, China.ORCID http://orcid.org/0009-0009-7836-9178
Hailun HeDepartment of Medical Aesthetics, The Third People's Hospital of Chengdu, Southwest Jiaotong University, Chengdu, China.
Haien WuDepartment of Dermatology, The Seventh People's Hospital of Shenyang, Shenyang, China.
Yichong WangDepartment of Dermatology, Shengjing Hospital of China Medical University, Shenyang, China.
Jingyu WangNational Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, The First Hospital of China Medical University and Key Laboratory of Immunodermatology, Ministry of Health and Ministry of Education, Shenyang, China.
Yan SunNational Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, The First Hospital of China Medical University and Key Laboratory of Immunodermatology, Ministry of Health and Ministry of Education, Shenyang, China.
Hexiao WangNational Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, The First Hospital of China Medical University and Key Laboratory of Immunodermatology, Ministry of Health and Ministry of Education, Shenyang, China.
Shulan YaoDepartment of Dermatology, Affiliated Hospital of Jining Medical University, Shandong, China.
Linlin ZhuDepartment of Dermatology, The Seventh People's Hospital of Shenyang, Shenyang, China.
Yi JiangCentral Laboratory, The First Hospital of China Medical University, Shenyang, China.
Xinze Cai *Central Laboratory, The First Hospital of China Medical University, Shenyang, China. xzcai@cmu.edu.cn.ORCID http://orcid.org/0000-0003-4998-2140
Yan Wu *Department of Dermatology, Shengjing Hospital of China Medical University, Shenyang, China. jlwuyan@126.com.

Funding

National Natural Science Foundation of China (National Science Foundation of China) No. 81401330National Natural Science Foundation of China (National Science Foundation of China) No. 82103745
6 · The paper itself

Abstract

Rosacea is a chronic inflammatory skin disorder linked to the antimicrobial peptide LL-37 and immune cells. STING, a key DNA-sensing adaptor, initiates innate immune responses, with excessive activation contributing to inflammation. This study investigates LAPTM5, a STING-interacting protein, and its role in rosacea. We observe elevated nuclear DNA fragmentation within the dermal lesions of rosacea patients and LL-37-induced rosacea-like mice. LAPTM5 and STING levels are upregulated in macrophages within rosacea lesions and LL-37-induced models, along with STING hyperactivation. LAPTM5 knockdown in macrophages reduces STING protein levels, signaling, and inflammatory responses under DMXAA and HT-DNA stimulation. LAPTM5 associates with STING and represses its K48- and K63-linked polyubiquitination, preventing proteasomal and lysosomal degradation, thereby maintaining STING stability at homeostasis and after activation. Both STING antagonist H-151 and LAPTM5 knockdown alleviate LL-37-induced rosacea-like phenotypes. These findings highlight LAPTM5 as a STING stabilizer, aggravating STING-driven inflammation in rosacea, offering insights for potential treatments.

Indexed as

Antimicrobial Cationic PeptidesCathelicidinsInflammationMembrane ProteinsRosaceaAnimalsFemaleHumansMacrophagesMaleMiceMice, Inbred C57BLSTING ProteinAntimicrobial Cationic PeptidesCathelicidinsMembrane ProteinsSTING1 protein, humanSting1 protein, mouseSTING Protein

Identifiers

PMID41087666
PMCPMC12521404

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.