ArticleNpj mental health research2026
Integrated proteomic, transcriptomic, and epigenomic profiling identifies SRA1 as a novel therapeutic target for postpartum depression.
Article in Npj mental health research, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postpartum depression (PPD) is among the most common complications of childbirth, and identifying novel treatments is vital. We aimed to identify potential drug targets for PPD by integrating the plasma proteome, transcriptome and epigenome. We designed a comprehensive analysis pipeline involving two-sample Mendelian randomisation (MR) (for proteins), colocalisation (for coding genes), and summary-based MR (SMR) (for mRNA and DNA methylation) to identify potential therapeutic targets for PPD. Genetic data on the plasma proteome were obtained from 4907 aptamers in 35,559 Icelanders and 7596 proteins in 828 FinnGen participants. The PPD genome-wide association study data were sourced from the Psychiatric Genomics Consortium (PGC) (Ncase = 17,339, Ncontrol = 53,426). A two-step MR approach was used to assess whether brain imaging-derived phenotypes (IDPs) and metabolites from blood, brain and cerebrospinal fluid mediated the observed effects. Across the two proteome datasets, the genetically predicted levels of 18 plasma proteins were nominally significantly associated with PPD, and the expression of steroid receptor RNA activator 1 (SRA1), a regulator of steroid hormone signalling, was significantly associated with PPD. SRA1, angiotensinogen (AGT, a key mediator of the renin-angiotensin and stress-response system), and glycerol-3-phosphate phosphatase (PGP, involved in lipid metabolism and cellular stress) showed increased colocalisation. The methylation of SRA1 at cg02434007 in the brain was associated with increased expression of SRA1 and a high risk of PPD, which aligns with the positive effect of SRA1 gene expression on PPD risk. Isoleucine (mediation proportion: 5.8%, p = 0.042) from blood metabolites and the IDP ICA100 edge 442 (mediation proportion: 7.6%, p = 0.044) may play mediating roles. This study reveals that SRA1 is a novel therapeutic target for PPD, which enhances the understanding of its molecular aetiology and the development of therapeutic strategies.
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.