ArticleJOR spine2025
E74-like ETS transcription factor 3 expression and regulation in human intervertebral disc.
Article in JOR spine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- The Role of Adipokines in Spinal Disease: A Narrative Review.JOR spine · 2025Review
- Role of oxidative stress in intervertebral disc degeneration: mechanisms, pathogenesis, and therapeutic strategies.Molecular biology reports · 2025Review
- E74-like ETS transcription factor 3 expression and regulation in human intervertebral disc.JOR spine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Intervertebral disc degeneration (IVDD) is one of the main causes of chronic low back pain. The degenerative process is often initiated by an imbalance between catabolic and anabolic pathways. Despite the large socio-economic impact, the initiation and progress of disc degeneration are poorly understood. Although intervertebral disc (IVD) and articular joint are not identical, their degenerative roads are remarkably similar. We, and another authors, previously demonstrated that E-74-like factor 3 (ELF3), a transcription factor induced by inflammatory mediators in various cell types including chondrocytes, is a central contributing factor for cartilage degradation. Thus, we aim to explore, for the first time, the expression, modulation, and the role of ELF3 in human IVD cells. Methods: The presence of ELF3 in healthy and degenerated IVD tissues was initially determined by immunohistochemistry in annulus fibrosus (AF) and nucleus pulposus (NP). mRNA and protein expression were measured, respectively, by RT-qPCR and Western blot in AF and NP IVD cells harvested from healthy individuals and IVDD patients. Overexpression of ELF3 was performed by transfection of AF IVDD cells with pESE-1: ELF3 expression vector or pCI: empty vector. Results: Our results unveiled, for the first time, the expression of ELF3 in IVD tissues. ELF3 is notably upregulated in degenerated tissues compared to those from healthy patients. In addition, the stimulation of IVDD AF cells with various proinflammatory stimuli, showed marked increase in both mRNA and protein expression of ELF3. ELF3 overexpression in AF IVDD cells resulted in the upregulation of proinflammatory and catabolic genes such as PTGS2, NOS2, LCN2, IL-6, MMP13, and ADAMTS-5; whereas, ELF3 silencing resulted in the opposite results. Conclusions: Our results support a novel role for ELF3 as a pro-inflammatory and pro-catabolic transcriptional mediator, whose targeting in IVD tissues might be of potential therapeutic relevance in disc degeneration.
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.