ArticleJournal of translational medicine2025
AT1R autoantibody impedes fetal hepatic glycogen synthesis by inhibiting PI3K/AKT signaling pathway during late gestation.
Article in Journal of translational medicine, 2025. 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
9 authors.
Funding
Abstract
backgroundFetal hepatic glycogen is essential for intrauterine development and postnatal metabolic adaptation. This study aimed to explore the impact of intrauterine exposure to angiotensin II type 1 receptor autoantibodies (AT1-AA) on fetal hepatic glycogen homeostasis and underlying mechanisms.
methodsAT1-AA-positive pregnant rat models were established by intravenous administration of AT1-AA on gestational days 13 and 15, with angiotensin II- and L-NAME-treated groups serving as controls. Serum levels of AT1-AA in pregnant rats were quantified using ELISA. Fetal hepatic glycogen content was evaluated through PAS staining and an anthrone-sulfuric acid assay kit. On gestational day 18, fetal livers were harvested for RNA sequencing. Alterations in signaling molecules in hepatocytes were analyzed by Western blot.
resultsUnlike the angiotensin II- and L-NAME-treated groups, which similarly induced placental ischemia and growth restriction, intrauterine exposure of AT1-AA uniquely reduced fetal hepatic glycogen content at gestational day 18. This reduction was attributed to impaired glycogen synthesis, as characterized by decreased GYS2 expression and glycogen synthase activity. Transcriptomic profiling revealed that suppression of the PI3K/AKT pathway was the predominant mechanism involved. Both in vivo and in vitro studies confirmed that AT1-AA-mediated PI3K/AKT inhibition occurs through AT1R activation. Either stimulation of the PI3K/AKT pathway or blockade of AT1R significantly restored glycogen synthesis.
conclusionsOur study identifies AT1-AA as a unique maternal factor that selectively impairs fetal hepatic glycogen storage via AT1R-mediated suppression of PI3K/AKT pathway.
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.