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Haozhang Huang

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Open access Aug 2026

Integrated proteomic, transcriptomic, and epigenomic profiling identifies SRA1 as a novel therapeutic target for postpartum depression

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.

Ming Chen, Qinlin Wei, Haowen Li et al. · 0 citations
Jul 2026

Sex-specific effects of depression on the incidence and risk factors for coronary heart disease: insights from multi-omics approaches.

AIMS Depression and coronary heart disease (CHD) exhibit notable sex disparities; however, the sex-specific effect of depression on the development of CHD remains unexplored. We explored these effects using multi-omics approaches. METHODS AND RESULTS In the UK Biobank cohort, we conducted sex-stratified survival analyses and multi-omics investigations, including sex-specific two-sample and one-sample Mendelian randomisation (MR) analyses, reproductive factor assessments, Life's Essential 8 factor evaluations, and plasma proteomics analysis. Depression was associated with a higher risk of CHD in females (adjusted hazard ratio [aHR]: 1.30; 95% confidence interval [CI]: 1.24-1.37) than in males (aHR: 1.14; 95% CI: 1.09-1.19; P-interaction < 0.001), compared with individuals without depression. Sex-specific two-sample and one-sample MR analyses showed that genetically predicted depression in females was causally related to CHD, but no causal effect was observed in males. Some key reproductive factors in females with depression were associated with a high risk of CHD. Among the Life's Essential 8 factors, poor control of nicotine exposure, blood pressure, body mass index, and blood glucose had an additional effect on CHD risk in females with depression compared with that in males (all P-interaction < 0.05). Analysis of the UKB-PPP cohort revealed 26 proteins with sex-specific associations, predominantly significant in females. CONCLUSIONS Our findings highlight significant sex differences in the effect of depression on CHD risk, which could inform sex-specific preventive strategies for reducing the cardiovascular burden in individuals with depression.

Haozhang Huang, Ming Chen, Xiaozhao Lu et al. · 0 citations