ArticleScientific reports2025
Comparison of necrotizing enterocolitis (NEC)-related apoptosis factors between preterm and full-term rats.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to determine whether there is a difference in the degree of apoptosis and the pathways leading to necrotizing enterocolitis (NEC) between preterm and full-term rat pups. To achieve this goal, we investigated the pathogenesis of NEC. premature Sprague‒Dawley (SD) rat pups delivered by cesarean section at a gestational age of 21 days (preterm group), as well as full-term SD rat pups four days after birth (full-term group). The pups were exposed to lipopolysaccharides (LPS) and hypoxia to induce necrotizing enterocolitis. Both preterm and full-term rats developed necrotizing enterocolitis. The results indicated that the degree of apoptosis was greater in both the preterm and full-term NEC groups than in the untreated preterm and full-term control groups. Compared with the control group, the full-term group also presented a reduction in Bcl-2 levels and an increase in the ratio. Moreover, the preterm group presented significantly increased RIPK1 expression, suggesting the induction of RIPK1-dependent apoptosis. These findings suggest that the pathophysiology of necrotizing enterocolitis induced by LPS + hypoxia is associated with the programmed cell death pathway. It appears that the apoptotic pathway of the Bax/Bcl-2 system is the main mechanism of necrotizing enterocolitis in full-term rats. In contrast, several other mechanisms, including TNF-α-induced apoptosis mechanism, may work together for necrotizing enterocolitis in preterm rats. However, further studies are needed to elucidate the differences in the pathogenesis of necrotizing enterocolitis development between preterm and full-term rats.
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.