Evidence map›Paper›PMID 41386837›Full record

ArticleJournal, genetic engineering & biotechnology2025

Causal correlation between inflammatory cytokines and hypertrophic scar based on two-sample Mendelian randomization.

Lujia Mao, Juan Huang, Yixun Zhang, Weiqiang Zhang, Xiaoxiang Wang, Ronghua Yang

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Article in Journal, genetic engineering & biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Lujia MaoThe Second Affiliated Hospital, School of Medicine, South China University of Technology, China; Department of Burn and Plastic Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Juan HuangCentral Sterile Services Department, Foshan Women and Children Hospital Affiliated to Guangdong Medical University, Foshan, Guangdong, China.
Yixun ZhangDepartment of Burn and Plastic Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Weiqiang ZhangThe First Clinical School of Medicine, Guangdong Medical University, Zhanjiang, Guangdong, China.
Xiaoxiang WangDepartment of Burn Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China. Electronic address: wangxx87@mail2.sysu.edu.cn.
Ronghua YangThe Second Affiliated Hospital, School of Medicine, South China University of Technology, China; Department of Burn and Plastic Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China. Electronic address: eyyangronghua@scut.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic scars result from the abnormal proliferation of fibroblasts and the accumulation of collagen after skin injury. In this process, inflammatory cytokines act as crucial regulators. The large - scale release of inflammatory cytokines aberrantly activates fibroblasts. It promotes the proliferation of fibroblasts and the synthesis of collagen, and simultaneously inhibits collagen degradation. The purpose of this study is to investigate the causal correlation between inflammatory cytokines and hypertrophic scars (HS). This study applied a two-sample Mendelian randomization approach (TSMR), leveraging summarized data gathered by genome-wide association studies (GWAS). The inflammatory cytokines (8293 samples) and hypertrophic scar (HS, 207,482 samples) summary data were analyzed to figure out whether there was a causal connection of the two.The inverse variance-weighted (IVW) method was implemented to undertake causal analysis, also sensitivity, heterogeneity, and pleiotropy analyses were performed to further evaluate the results' stability and dependability.Two inflammatory cytokines, IL-2 and CCL4, were identified as being associated with HS. The IVW analysis demonstrated a positive relationship between IL-2 and the risk of HS (OR = 1.51, 95 % CI = 1.06-2.15, P = 0.02), indicating that IL-2 is a risk factor for hypertrophic scarring, with elevated levels potentially promoting disease progression. In contrast, CCL4 was negatively associated with HS risk (OR = 0.86, 95 % CI = 0.74-0.99, P = 0.03), pointing to the fact CCL4 might function as a protective agent, where lower levels of CCL4 could inhibit scar formation. Sensitivity analyses verified the dependability of the TSMR results (P > 0.05). Our MR analysis indicates a causal correlation between inflammatory cytokines and hypertrophic scars. Specifically, IL-2 promotes hypertrophic scar formation, whereas CCL4 exerts a protective effect, reducing the risk of scar formation. These discoveries imply that inflammatory cytokines have a considerable part to play in the pathogenesis of hypertrophic scarring through modulating its formation.

Indexed as

Causal relationshipHypertrophic scarInflammatory cytokinesTwo-sample Mendelian randomization

Identifiers

PMID41386837
PMCPMC12481052

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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.