ArticleScience advances2020
Actomyosin contractility confers mechanoprotection against TNFα-induced disruption of the intervertebral disc.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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
25 citing papers in PubMed, 35 citations in OpenAlex.
- Innovative Sutureless Fabrication Strategy for Tissue-Engineered Pediatric Heart Valves Using an Evolutive Support System.Annals of biomedical engineering · 2026Article
- Immune system expression profiling in patients experiencing low back pain: A pilot study.PM & R : the journal of injury, function, and rehabilitation · 2026Observational
- CEST MRI: Translational prospects for intervertebral disc degeneration - from basic research to clinical applications.Journal of orthopaedic translation · 2026Review
- Integrating cells, scaffolds, and molecular regulation: a mechanobiological and translational review of bioengineering therapies for intervertebral disc degeneration.Frontiers in bioengineering and biotechnology · 2026Review
- Bioinformatic analysis of glycosylation-related genes in intervertebral disc degeneration and their roles in immune infiltration and diagnostic models.Scientific reports · 2025Article
- Macrophage Subtypes Distinctly Impact Intervertebral Disc Inflammation and Extracellular Matrix Composition.JOR spine · 2025Article
- Exploring Mechanotransduction and Inflammation in Human Cartilaginous Endplate Cells in Blended Collagen-Agarose Hydrogels Under Cyclic Compression.Gels (Basel, Switzerland) · 2025Article
- TNF induces catabolism in human cartilaginous endplate cells in 3D agarose culture under dynamic compression.Scientific reports · 2025Article
- Data-driven analysis for the evaluation of cortical mechanics of non-adherent cells.Scientific reports · 2025Article
- Revolutionizing the treatment of intervertebral disc degeneration: an approach based on molecular typing.Journal of translational medicine · 2025Article
- Actin contraction controls nuclear blebbing and rupture independent of actin confinement.Molecular biology of the cell · 2024Article
- The pathogenesis and targeted therapies of intervertebral disc degeneration induced by cartilage endplate inflammation.Frontiers in cell and developmental biology · 2024Review
- Article
- Intervertebral Disc-on-a-ChipAdvanced materials technologies · 2023Article
- Review
- Spheroid-Based Tissue Engineering Strategies for Regeneration of the Intervertebral Disc.International journal of molecular sciences · 2022Review
- New Progress in Basic Research of Macrophages in the Pathogenesis and Treatment of Low Back Pain.Frontiers in cell and developmental biology · 2022Review
- Immuno-Modulatory Effects of Intervertebral Disc Cells.Frontiers in cell and developmental biology · 2022Review
- Naringin protects human nucleus pulposus cells against TNF-Oxidative medicine and cellular longevity · 2022Article
- Inhibition of toll-like receptor 4 protects against inflammation-induced mechanobiological alterations to intervertebral disc cells.European cells & materials · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation triggers degradation of intervertebral disc extracellular matrix (ECM), a hallmark of disc degeneration that contributes to back pain. Mechanosensitive nucleus pulposus cells are responsible for ECM production, yet the impact of a proinflammatory microenvironment on cell mechanobiology is unknown. Using gain- and loss-of-function approaches, we show that tumor necrosis factor-α (TNFα)-induced inflammation alters cell morphology and biophysical properties (circularity, contractility, cell stiffness, and hydraulic permeability) in a mechanism dependent on actomyosin contractility in a three-dimensional (3D) culture. We found that RhoA activation rescued cells from TNFα-induced mechanobiological disruption. Using a novel explant-in-hydrogel culture system, we demonstrate that nuclear factor kappa-B nuclear translocation and transcription are mechanosensitive, and its downstream effects on ECM degradation are regulated by actomyosin contractility. Results define a scaling relationship between circularity, contractility, and hydraulic permeability that is conserved from healthy to inflammatory microenvironments and is indicative of cell mechanobiological control across scales in 3D.
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.