ArticleMedicine2026
Transcriptome data combined with two-sample Mendelian randomization reveal IRF1 and PRKD1 as UPR-related key regulators in intervertebral disc degeneration.
Article in Medicine, 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
8 authors.
Funding
Abstract
Intervertebral disc degeneration (IDD) is a leading cause of chronic low back pain, yet the molecular mechanisms driving its progression remain incompletely defined. Emerging evidence suggests that endoplasmic reticulum stress and the unfolded protein response (UPR) may play critical roles in disc cell dysfunction. Transcriptomic datasets (GSE70362 and GSE56081) from human nucleus pulposus tissues were integrated to identify UPR-related differentially expressed genes. Functional enrichment, gene set enrichment analysis, and gene set variation analysis analyses were performed to explore associated biological pathways. Protein-protein interaction networks, transcription factor-target predictions, and immune infiltration analyses were conducted. Two-sample Mendelian randomization was applied to assess potential causal relationships between UPR-related genes and IDD. Key genes were further validated using independent datasets and single-cell RNA sequencing data. A total of 26 UPR-related differentially expressed genes were identified, and protein-protein interaction network analysis with hub gene screening highlighted IRF1, PRKD1, CCND1, and PDLIM1 as central regulators. Two-sample Mendelian randomization confirmed the causal associations of IRF1 and PRKD1 with IDD risk. Immune infiltration analysis revealed significant correlations between UPR-related genes and the activity of macrophages and T cells. Single-cell RNA sequencing further validated the differential expression and cell-type specificity of IRF1 and PRKD1 in degenerated nucleus pulposus tissues. This integrative multi-omics and Mendelian randomization study identifies IRF1 and PRKD1 as UPR-related drivers of IDD. These findings provide potential biomarkers and therapeutic targets for IDD management.
Indexed as
Identifiers
What Socratic 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 Socratic graph.