ArticleJOR spine2025
Transient Receptor Potential Vanilloid 4 Knockdown Decreases Extracellular Matrix Synthesis via Autophagy Suppression in the Rat 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
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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.
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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.
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Who cites it
3 citing papers in PubMed.
- Organ-on-a-Chip Technology: Advances in Modeling Inflammation, Neurovascularization and Nociception in Human Intervertebral Disc Degeneration.Smart medicine · 2026Review
- Article
- From mechanotransduction to manual therapy: advances in piezo/TRP channels and lumbar degeneration.Frontiers in physiology · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Transient receptor potential vanilloid 4 (TRPV4) has been identified as a Ca Methods: In vitro study: Small interfering RNA (siRNA) was applied to knockdown TRPV4 by the reverse transfection method in rat disc NP cells. Expression of TRPV4, AMPK/mTOR pathway-related markers, and autophagy markers were measured by Western blotting (WB). Next, ECM metabolism was assessed under serum starvation and/or proinflammatory interleukin-1 beta (IL-1β) stimulation. In vivo study: TRPV4 and control siRNAs were injected into rat discs. To confirm in vivo transfection, WB for TRPV4 was conducted in rat disc NP-tissue protein extracts 2, 28, and 56 days after injection. Furthermore, 24-h temporary static compression-induced disruption of TRPV4 siRNA-injected discs was observed by radiography, histomorphology, and immunofluorescence. Results: In vitro study: In disc cells, three different TRPV4 siRNAs consistently suppressed autophagy with TRPV4 protein knockdown (mean 33.2% [95% CI: -50.8, -15.5], 44.1% [-61.7, -26.4], 58.3% [-76.0, -40.7]). ECM metabolism was significantly suppressed by TRPV4 RNAi under proinflammatory IL-1β stimulation. In vivo study: The WB displayed sustained decreases in TRPV4 protein expression 2, 28, and 56 days after injection. Under the loaded condition, TRPV4 siRNA-injected discs presented radiographic height loss ([-31.7, -7.75]), histomorphological damage ([0.300, 4.70]), and immunofluorescent suppression of autophagy ([1.61, 20.5]) and ECM metabolism ([-25.2, -6.41]) compared to control siRNA-injected discs at 56 days. Conclusions: The TRPV4 could be a therapeutic target for intervertebral disc diseases via modulating autophagy.
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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.