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已发表论文
银屑病皮肤中不饱和脂肪酸代谢重编程驱动炎症并预测对生物疗法的反应
Authors Miao H , Guan X, Li L, Wang L, Luo Y
Received 27 September 2025
Accepted for publication 5 December 2025
Published 18 December 2025 Volume 2025:18 Pages 3497—3509
DOI https://doi.org/10.2147/CCID.S569278
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Monica K. Li
Haijun Miao,* Xiaojuan Guan,* Liangliang Li, Lixing Wang, Yang Luo
Department of Dermatology, The 940th Hospital of Joint Logistic Support Force of Chinese PLA, Lanzhou, Gansu Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yang Luo, Department of Dermatology, The 940th Hospital of Joint Logistic Support Force of Chinese PLA, Lanzhou, Gansu Province, People’s Republic of China, Tel +86 0931 8994193, Email lytmmu@163.com
Purpose: Psoriasis is frequently associated with dyslipidemia, yet the role of specific unsaturated fatty acid (UFA) metabolic pathways in disease pathogenesis and treatment response remains poorly understood. This study aimed to characterize the landscape of UFA metabolic reprogramming in psoriasis and evaluate its clinical relevance for predicting response to biologic therapy.
Patients and Methods: We performed an integrated multi-omics analysis incorporating transcriptomic data from human psoriatic lesions, single-cell RNA sequencing, and lipidomic profiling. Gene set variation analysis (GSVA) was used to evaluate UFA pathway activity. Logistic regression and LASSO were employed for biomarker selection and predictive modeling.
Results: We identified eight significantly dysregulated UFA metabolic pathways in psoriatic lesions, six of which were associated with key pathogenic processes in psoriasis. All pathways were reversibly modulated by biologic agents targeting TNF-α, IL-12/23, and IL-17A. We derived a three-gene biomarker signature (PLA2G4D, PLA2G4A, and FADS2) that robustly predicts response to IL-12/23 inhibition prior to treatment initiation (AUC = 0.902). Single-cell RNA sequencing revealed keratinocytes as the primary cellular contributors to UFA metabolism and identified an expanded PLA2G4D-high keratinocyte subpopulation in psoriatic skin, which was associated with the accumulation of Lysophosphatidylcholine (LysoPC) and Lysophosphatidylethanolamine (LysoPE).
Conclusion: Our findings elucidate the pathway-level metabolic basis of psoriasis inflammation and provide a clinically applicable tool for predicting response to biologic therapy. The results highlight the importance of UFA metabolic reprogramming in psoriatic pathogenesis and offer new avenues for treatment personalization.
Keywords: unsaturated fatty acid metabolism, psoriasis, biologic therapy, predictive biomarkers, keratinocyte, PLA2G4D
Department of Dermatology, The 940th Hospital of Joint Logistic Support Force of Chinese PLA, Lanzhou, Gansu Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yang Luo, Department of Dermatology, The 940th Hospital of Joint Logistic Support Force of Chinese PLA, Lanzhou, Gansu Province, People’s Republic of China, Tel +86 0931 8994193, Email lytmmu@163.com
Purpose: Psoriasis is frequently associated with dyslipidemia, yet the role of specific unsaturated fatty acid (UFA) metabolic pathways in disease pathogenesis and treatment response remains poorly understood. This study aimed to characterize the landscape of UFA metabolic reprogramming in psoriasis and evaluate its clinical relevance for predicting response to biologic therapy.
Patients and Methods: We performed an integrated multi-omics analysis incorporating transcriptomic data from human psoriatic lesions, single-cell RNA sequencing, and lipidomic profiling. Gene set variation analysis (GSVA) was used to evaluate UFA pathway activity. Logistic regression and LASSO were employed for biomarker selection and predictive modeling.
Results: We identified eight significantly dysregulated UFA metabolic pathways in psoriatic lesions, six of which were associated with key pathogenic processes in psoriasis. All pathways were reversibly modulated by biologic agents targeting TNF-α, IL-12/23, and IL-17A. We derived a three-gene biomarker signature (PLA2G4D, PLA2G4A, and FADS2) that robustly predicts response to IL-12/23 inhibition prior to treatment initiation (AUC = 0.902). Single-cell RNA sequencing revealed keratinocytes as the primary cellular contributors to UFA metabolism and identified an expanded PLA2G4D-high keratinocyte subpopulation in psoriatic skin, which was associated with the accumulation of Lysophosphatidylcholine (LysoPC) and Lysophosphatidylethanolamine (LysoPE).
Conclusion: Our findings elucidate the pathway-level metabolic basis of psoriasis inflammation and provide a clinically applicable tool for predicting response to biologic therapy. The results highlight the importance of UFA metabolic reprogramming in psoriatic pathogenesis and offer new avenues for treatment personalization.
Keywords: unsaturated fatty acid metabolism, psoriasis, biologic therapy, predictive biomarkers, keratinocyte, PLA2G4D