ArticleMaterials today. Bio2026
Hydrogels Targeting Mechanical-biological signaling transitions of interleukin-33 alleviates intervertebral-disc degeneration.
Article in Materials today. Bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting AMPK signaling in nucleus pulposus cells ameliorates spaceflight microgravity-induced intervertebral disc degeneration.Cell death and differentiation · 2026Article
- From mechanotransduction to manual therapy: advances in piezo/TRP channels and lumbar degeneration.Frontiers in physiology · 2026Review
- Mechanotransduction in intervertebral disc degeneration: from compartment-specific sensors to translational frontiers.Frontiers in bioengineering and biotechnology · 2026Review
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Authors and funding
13 authors.
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Abstract
Mechanical-biological signaling transitions (MBSTs) cause intervertebral-disc degeneration (IVDD). The key to MBSTs lies in nucleus pulposus cells (NPCs), but it is not yet fully understood, and relevant therapeutic targets and strategies are lacking. In this study, we found that the key mechanobiological-signaling factor interleukin-33 (IL-33) played an important role in stress-induced IVDD through a piezo-type mechanosensitive ion channel component 1 (PIEZO1)-mediated positive-feedback loop. Specifically, analysis of clinical samples showed that IL-33 was significantly upregulated in NPCs from IVDD patients and that compressive-stress stimulation further enhanced IL-33 expression via the PIEZO1 pathway, thereby accelerating disc degeneration. To discover the underlying mechanism, we fabricated the transfection nanoparticles formed by benzoboric acid-modified polyethyleneimine (PEI-PBA) with
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