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Multi-omic insights into mitochondrial dysfunction and prostatic disease: evidence from transcriptomics, proteomics,
Binbin Gong1,2,3, Feixiang Yang1,2,3, Ning Zhang4
1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Frontiers in Genetics
|September 8, 2025
Summary
This study integrates multi-omics data to identify mitochondrial genes linked to benign prostatic hyperplasia (BPH), prostatitis, and prostate cancer (PCa). Key genes and metabolic pathways are highlighted as potential therapeutic targets for these prostatic diseases.
Area of Science:
- Genomics and Systems Biology
- Mitochondrial Biology
- Urology
Background:
- Prostatic diseases, including benign prostatic hyperplasia (BPH), prostatitis, and prostate cancer (PCa), represent significant health concerns.
- Mitochondrial dysfunction is implicated in prostatic diseases, but comprehensive multi-omics integration is needed to elucidate mechanisms.
- Previous single-omics studies offer insights, necessitating advanced approaches for deeper understanding and therapeutic target identification.
Purpose of the Study:
- To perform a genome-wide meta-analysis for prostatic diseases using GWAS data.
- To integrate multi-omics data (eQTLs, pQTLs, mQTLs) to identify mitochondrial dysfunction-related genes associated with prostatic diseases.
- To explore mediating pathways involving metabolites and immune factors in the interaction between mitochondrial genes and prostatic diseases.
Main Methods:
- Genome-wide association studies (GWAS) meta-analysis on FinnGen and UK Biobank data for prostatic diseases.
- Integration of quantitative trait loci (QTL) across gene expression (eQTLs), protein abundance (pQTLs), and DNA methylation (mQTLs) for 1,244 mitochondrial genes (MitoCarta 3.0).
- Prioritization of genes into confidence tiers and mediation analyses with metabolomics and immunomics data.
Main Results:
- DCXR identified as a Tier 1 gene for BPH, supported by multi-omics signatures.
- Identified additional genes for BPH (NOA1, ELAC2, ACAT1), prostatitis (TRMU, SFXN5), and PCa (MRPL24, NDUFS6, PUS1, NBR1, GLOD4, PCBD2).
- Discovered 8, 4, and 13 mediating metabolites for BPH, prostatitis, and PCa, respectively, without immune involvement.
Conclusions:
- Highlights the critical roles of mitochondrial dysfunction-related genes in prostatic diseases.
- Identifies specific genes (e.g., DCXR) and metabolic pathways as potential therapeutic targets.
- Emphasizes the power of multi-omics integration for uncovering disease mechanisms and guiding future treatments.
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