ArticleNature metabolism2026
NNMT enhances hyperandrogenism in polyendocrine metabolic ovarian syndrome through epigenetic remodelling.
Article in Nature metabolism, 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
14 authors.
Funding
Abstract
Polyendocrine metabolic ovarian syndrome (PMOS) features intertwined reproductive, endocrine and metabolic defects, yet its initiating mechanisms remain incompletely understood. Here we show that an epigenetic mechanism driven by nicotinamide N-methyltransferase (NNMT) in granulosa cells contributes to disease progression in PMOS. We observe that Nnmt overexpression in mouse granulosa cells reduces histone H3 lysine 27 trimethylation (H3K27me3), leading to increased retinoic acid receptor beta (RARB) expression. RARB, in turn, amplifies ovarian androgen synthesis. The resulting androgen excess further suppresses H3K27me3, locking cells into a feedforward loop that sustains hyperandrogenism and disrupts follicle development. Pharmacological inhibition of NNMT restores H3K27me3, disrupts the RARB-androgen feedback circuit, and ameliorates both metabolic and hormonal phenotypes in PMOS models. Our findings suggest NNMT as a regulator of PMOS through metabolic and epigenetic reprogramming. The NNMT-H3K27me3-RARB-androgen axis emerges as a mechanistic nexus linking methionine and epigenetic dysregulation to PMOS pathogenesis and represents a tractable therapeutic target.
Identifiers
42888303What 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.