ArticleEnvironmental toxicology2026
Mono(2-Ethylhexyl) Phthalate Induces Inflammatory and Angiogenic Alterations Mediated by the PI3K/AKT Pathway in HTR-8/SVneo Trophoblastic Cells.
Article in Environmental toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- A Perfect Storm of Pollutants: Environmental Mixtures in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2026Review
- Mono(2-Ethylhexyl) Phthalate Induces Inflammatory and Angiogenic Alterations Mediated by the PI3K/AKT Pathway in HTR-8/SVneo Trophoblastic Cells.Environmental toxicology · 2026Article
- Prenatal Exposure to Mixtures of Nonpersistent Endocrine-Disrupting Chemicals and Angiogenic Biomarkers, Placental Function, and Fetal Growth.Environmental science & technology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Exposure to mono(2-ethylhexyl) phthalate (MEHP) during pregnancy has been associated with adverse pregnancy and birth outcomes characterized by extravillous trophoblast (EVT) abnormal function. Previous reports have suggested that MEHP can activate the PI3K/AKT pathway in EVT cells, a pathway known to regulate inflammation and angiogenesis in these cells. However, the molecular effects of MEHP on crucial EVT functions such as inflammatory and angiogenic homeostasis remain unexplored. This study aimed to characterize the role of the PI3K/AKT pathway as a mechanism of action of MEHP activity, as well as its effects on inflammatory and angiogenic soluble molecules in HTR-8/Svneo EVT human-derived cells. The results showed that a low (5 μM) MEHP concentration increased AKT phosphorylation, but a high (200 μM) concentration did not. Conversely, a high MEHP concentration, but not a low concentration, promoted nuclear translocation of p65 in a PI3K-dependent manner. Notably, distinct patterns of cytokines were transcriptionally and secretorily activated by high and low concentrations of MEHP. IL1B, CXCL8, and TNF were transcriptionally upregulated by MEHP 5 μM, while gene expression and secretion of IL-6 were induced by MEHP 200 μM, suggesting a biphasic inflammatory dose response. In addition, both MEHP concentrations upregulated the expression of angiogenic molecules (VEGF, PGF, and ANGPTL4) and impaired migration and tube formation in HTR-8/Svneo cells. Both inflammatory and angiogenic responses induced by MEHP were inhibited by the PI3K inhibitor LY294002. Collectively, these data demonstrate that MEHP induces inflammation and impairs angiogenesis partly via PI3K/AKT in HTR-8/SVneo cells. These findings may help to understand previous clinical associations between MEHP exposure and placental pathophysiology.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.