Evidence map›Paper›PMID 40151075›Full record

ArticleCombinatorial chemistry & high throughput screening2026

Exploring Mechanisms of Ephx2 in Treating Atherosclerosis Using Independent Cascade Model and Adverse Outcome Pathways.

Caiyuzhen Zhang, Yuanwen Dai, Yong Chen, Bo Cao, Jinbing An, Wei Pang

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Article in Combinatorial chemistry & high throughput screening, 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

Authors and funding

6 authors.

Caiyuzhen ZhangJiangxi Normal University, 100875, China.
Yuanwen DaiJiangxi Normal University, 100875, China.
Yong ChenJiangxi Normal University, 100875, China.
Bo CaoDepartment of Health Informatics and Management, School of Health Humanities, Peking University, Beijing, 100191, China.
Jinbing AnDepartment of Health Informatics and Management, School of Health Humanities, Peking University, Beijing, 100191, China.
Wei PangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.

Funding

Natural Science Foundation of Beijing Municipality 7212057
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a leading cause of cardiovascular diseases, characterized by lipid accumulation in arterial walls. The gene Ephx2, which encodes soluble epoxide hydrolase (sEH), is implicated in AS development, but its precise mechanisms and therapeutic potential are not fully understood.

objectivesThis study aimed to analyze gene expression data from low-density lipoprotein receptor knockout (LDLR-/-) and LDLR

methodsA directed compound-protein interaction network was constructed based on these genes and related pathways from the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. In the end, through resistance distance (RD) between any two nodes in this network, the Independent Cascade (IC) model was applied to explore Ephx2 mechanisms in AS, such as important Adverse Outcome Pathways (AOPs).

resultsSeveral AOPs were identified as critical in AS treatment via Ephx2. The key AOPs included inflammatory response and cytokine release, cholesterol deposition and oxidation, disruption of plaque stability, smooth muscle cell proliferation and migration, and platelet activation and coagulation. Within the top AOPs of inflammatory response and cytokine release, potential target genes were identified, such as Mapk3, Pik3cd, Gnai2, Mapk10, Arnt, and RhoA. Critical paths from Ephx2 to these target genes were established, suggesting mechanisms by which Ephx2 may influence AS pathogenesis.

conclusionBy defining the AS network and corresponding RD, this study elucidates potential mechanisms by which Ephx2 affects AS through specific KEGG pathways, AOPs, and target genes. These findings enhanced the understanding of AS pathogenesis and highlighte potential targets like Mapk3 for developing therapeutic strategies in AS prevention and treatment.

Indexed as

AtherosclerosisEpoxide HydrolasesAnimalsMiceMice, KnockoutReceptors, LDLEphx2 protein, mouseEpoxide HydrolasesReceptors, LDLadverse outcome pathwayAtherosclerosisEphx2independent cascade modelresistance distancesoluble epoxide hydrolase

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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.