ArticleScientific reports2026
Integrative bioinformatics analyses of mitochondrial dysfunction-related genes in human non-obstructive azoospermia.
Article in Scientific reports, 2026. 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.
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Non-obstructive azoospermia (NOA) is the severest form of male infertility. This study aimed to identify core genes associated with mitochondrial dysfunction and regulatory networks in NOA, providing potential diagnostic biomarkers and therapeutic targets for NOA. We identified mitochondrial dysfunction-related hub genes by analyzing three testis transcriptome datasets, and further confirmed their diagnostic value, differential expression in clinical specimens, and immune infiltration associations. For GSE108886 and GSE145467, 35 mitochondrial dysfunction-related differentially expressed genes (MD-DEGs, 10 upregulated and 25 downregulated) were obtained. And 6 common hub genes (COX7A1, COX7A2, COX7B2, MRPS15, AURKAIP1, and PDHA2) were identified. hsa-miR-12,116, hsa-miR-296-5p, and transcription factors (FOXA1, FOXC1, GATA2, SRF) simultaneously targeted two hub MD-DEGs. Diagnostic model incorporating COX7A1, COX7A2, AURKAIP1 and MRPS15 presented preliminary diagnostic efficacy with AUC value of 0.930 (95% CI [0.835-1.000]). Subsequently, RT-qPCR confirmed upregulation of COX7A1 (P < 0.05) and downregulation of COX7A2, COX7B2, MRPS15, AURKAIP1 and PDHA2 (P < 0.05 for all) in NOA patients. In addition, T cells CD8 and Mast cells resting were enriched in NOA patients. MD-DEGs including COX7A1, COX7A2, MRPS15 and AURKAIP1 may play pivotal roles in NOA pathogenesis, and could serve as a pre-biopsy screening tool to stratify patients and monitor therapeutic responses for NOA.
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.