ArticleFrontiers in cell and developmental biology2026
Fluid percussion trauma to the placental trophoblast triggers multifaceted injury mechanisms, including mitochondrial stress response, immune dysregulation, cytoskeletal, endothelial, and angiogenic signaling cascades.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Trauma is the leading cause of non-obstetrical maternal death and is linked to adverse pregnancy outcomes, including placental abruption, preterm birth, and stillbirth. Although placental injury is a known consequence of maternal trauma, understanding its direct effect on trophoblast function remains limited. This study aims to examine the cellular effects of mechanical trauma on human trophoblasts Methods: Human trophoblast cells (HTR-8/SVneo) were cultured and exposed to controlled mechanical trauma using a fluid percussion injury (FPI) model, previously validated in traumatic brain injury research. Cell viability was measured 48 h after injury with a fluorometric assay kit. Immunofluorescence and Western blot analyses were carried out to assess the levels of mitochondrial markers (TOM20, COX1, VDAC1) and the antiangiogenic factor sFlt-1. Results: Trophoblasts subjected to trauma exhibited reduced viability compared with controls. Expression of sFlt-1 and SDHA increased in injured cells, indicating a cellular stress response. Western blot results revealed a twofold decrease in TOM20 levels and a slight reduction in VDAC1 levels, while COX1 levels remained unchanged. Moreover, next-generation sequencing of trophoblasts after trauma showed altered gene expression involving several injury pathways, including mitochondrial stress response, immune dysregulation, cytoskeletal changes, endothelial and angiogenic signaling pathways, calcium signaling, metabolic imbalance, and inflammation. These results suggest that mechanical trauma causes mitochondrial dysfunction and disrupts angiogenic signaling in trophoblasts. Discussion: Trauma induces significant mitochondrial changes and cellular stress, characterized by reduced viability, decreased TOM20 and VDAC1 levels, and increased sFlt-1 and SDHA levels. These patterns resemble those seen in hypoxia-related placental disorders such as preeclampsia, fetal distress, and placental abruption. Understanding these mechanisms may help clarify how maternal trauma contributes to adverse pregnancy outcomes. Further studies using
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.