ArticleBiological research2025
FGA, a new target of histone acetylation, inhibits apoptosis of granulosa cells in follicles.
Article in Biological research, 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.
- Digitoxin-induced apoptosis in ovarian granulosa cells disrupts follicular development and impairs reproductive performance.Journal of ovarian research · 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
12 authors.
Funding
Abstract
Granulosa cells (GCs) are the main supporting cells for follicles, and histone acetylation has been reported to regulate follicular development. However, the mechanism of histone acetylation regulating follicular development is still unclear in GCs. In this study, we found that FGA, fibrinogen alpha chain, mediated the survival and fate of GCs. Knockdowns of HDAC1 and HDAC3 significantly inhibited the mRNA level of FGA, while knockdown of HDAC2 notably decreased the protein level of FGA. Moreover, knockdown of HDAC2 repressed the chromatin accessibility and the enrichment level of H3K9ac at -1350/-1454 bp of FGA. In addition, FGA promoted GCs proliferation and cycle progression by up-regulating the expressions of PCNA and CCNE1, whereas it inhibited apoptosis by suppressing the expression of Caspase3. In vitro, FGA was likely to promote follicular development of pigs. In mice, FGA inhibited the apoptosis of GCs and increased the number of corpora lutea, as a result, elevating estradiol levels and advancing the day of pubertal initiation. Both in vitro and in vivo experiments, FGA promoted follicular development by up-regulating PCNA and CCNE1, while inhibited follicular apoptosis by down-regulating Caspase3 and Caspase9. Overall, knockdown of HDAC2 repressed transcription by reducing chromatin accessibility and decreasing H3K9ac binding at the FGA promoter. FGA inhibited apoptosis of GCs by suppressing the expression of Caspase3 and promoted follicular development. This study showed that FGA is a novel target for histone acetylation to regulate follicular development in mammals.
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.