ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2024
Role of the soluble epoxide hydrolase in keratinocyte proliferation and sensitivity of skin to inflammatory stimuli.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Artificial Sweeteners and Autoimmune Diseases: Insights From Integrative Bioinformatics and Mendelian Randomization.Food science & nutrition · 2026Article
- Design, Synthesis, and Structure-Activity Relationships of Substituted Phenyl Cyclobutylureas as Potential Modulators of Inflammatory Responses.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Bioinformatics analyses of comorbid mechanisms between psoriasis and type 2 diabetes mellitus.Scientific reports · 2025Article
- DGAT2 reduction and lipid dysregulation drive psoriasis development in keratinocyte-specific SPRY1-deficient mice.JCI insight · 2025Article
- Integrative cardiovascular disease therapy: Linoleic acid restriction, enhanced external counterpulsation, and emerging nanotherapies.World journal of cardiology · 2025Review
- Arachidonic acid metabolism regulates the development of retinopathy of prematurity among preterm infants.Journal of neurochemistry · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
The lipid content of skin plays a determinant role in its barrier function with a particularly important role attributed to linoleic acid and its derivatives. Here we explored the consequences of interfering with the soluble epoxide hydrolase (sEH) on skin homeostasis. sEH; which converts fatty acid epoxides generated by cytochrome P450 enzymes to their corresponding diols, was largely restricted to the epidermis which was enriched in sEH-generated diols. Global deletion of the sEH increased levels of epoxides, including the linoleic acid-derived epoxide; 12,13-epoxyoctadecenoic acid (12,13-EpOME), and increased basal keratinocyte proliferation. sEH deletion (sEH
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Registered trials
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.