ArticleFrontiers in pharmacology2026
Hepatic lipid accumulation induced by mono-(2-ethylhexyl) phthalate and potential ERBB2-associated inflammatory signaling in NAFLD.
Article in Frontiers in pharmacology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Background: The primary active metabolite of di (2-ethylhexyl) phthalate (DEHP), mono (2-ethylhexyl) phthalate (MEHP), has received increasing attention due to its association with metabolic liver injury. However, the mechanisms underlying its involvement in nonalcoholic fatty liver disease remain poorly understood. Methods: This study employed an integrative approach combining network toxicology, machine learning, and molecular docking analyses to systematically investigate the potential molecular mechanisms of MEHP-related NAFLD and to identify candidate targets potentially involved in disease progression. Immune infiltration analysis and Results: Multidimensional analyses identified ERBB2 as a candidate gene worthy of further investigation. Immune infiltration analysis suggested that ERBB2 may be associated with alterations in the hepatic immune microenvironment, whereas molecular docking analysis indicated a potential interaction between MEHP and ERBB2. Further Conclusion: From the perspective of inflammation and immune regulation, this study proposes that ERBB2 may be involved in MEHP-induced NAFLD, providing a new theoretical basis for toxicological research on environment-related NAFLD.
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