Evidence map›Paper›PMID 42005973›Full record

ArticleClinical, cosmetic and investigational dermatology2026

Decoding the Causal Effects of Blood-Related Phenotypes in Hypertrophic Scars and Keloids: A Mendelian Randomization Study.

Fang Zhou, Gao Zeng

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Article in Clinical, cosmetic and investigational dermatology, 2026. 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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5 · Who and what money

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2 authors.

Fang ZhouDepartment of Plastic and Reconstructive Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, People's Republic of China.
Gao ZengDepartment of Plastic and Reconstructive Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, People's Republic of China.

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6 · The paper itself

Abstract

Background: Hypertrophic scars (HS) and keloids are pathological outcomes of aberrant wound healing. Their association with systemic physiological factors remains unclear. Mendelian randomization (MR) uses genetic variants as instrumental variables (IVs) to infer causality, minimizing confounding factors. Objective: In this study, we aim to investigate the causal effects of blood-related phenotypes, including blood cell counts, blood pressure, lipids, and glucose, on the risk of HS and keloids using a two-sample MR method. Methods: Genetic instruments for exposures were obtained from publicly available GWAS summary statistics, while outcome data were sourced from the FinnGen database and GWAS Catalog. The IVs were selected based on genome-wide significance (P < 5 × 10 Results: Genetically predicted higher leukocyte (OR: 1.175, 95% CI: 1.049-1.315, P = 0.005) and neutrophil counts (OR: 1.177, 95% CI: 1.040-1.332, P = 0.010) were causally associated with increased keloid risk. Conversely, lower systolic blood pressure (SBP) (OR: 0.709, 95% CI: 0.537-0.938, P = 0.016) and diastolic blood pressure (DBP) (OR: 0.732, 95% CI: 0.565-0.949, P = 0.018) were causally linked to higher HS risk, and lower SBP (OR: 0.760, 95% CI: 0.622-0.928, P = 0.007) was associated with increased keloid risk. No causal relationships were found for other blood cells, lipids, or glucose with either scar type. Sensitivity analyses did not indicate substantial heterogeneity or horizontal pleiotropy, supporting the robustness of the main findings. Conclusion: Our study suggests the causal effects of blood-related phenotypes in HS and keloids by using an MR method. Our results offer novel etiological insights and a potential perspective for scar-related intervention.

Indexed as

blood phenotypescausal inferencehypertrophic scarskeloidsMendelian randomization

Identifiers

PMID42005973
PMCPMC13091637

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