ArticleMaterials today. Bio2025
Photothermal-triggered NO-releasing nanofiber membrane mitigates intervertebral disc degeneration via inflammation inhibition and matrix stabilization.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed.
- Proteostasis Dysfunction and Heat Shock Protein Networks in Intervertebral Disc Degeneration: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- A manganese-luteolin co-loaded antioxidant hydrogel for synergistic alleviation of oxidative stress and immunomodulation in intervertebral disc degeneration.Materials today. Bio · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc-related low back pain represents a major source of chronic pain. Due to the inflammatory microenvironment and impaired extracellular matrix (ECM) synthesis in intervertebral disc degeneration (IVDD), annulus fibrosus (AF) injuries have limited healing capacity. Effective AF repair thus requires modulation of the inflammatory state, promotion of ECM deposition, and enhancement of cellular migration. In this study, we developed a multifunctional photothermal nanofibrous membrane system by electrospinning biocompatible chitosan (CS) and polyvinyl alcohol (PVA) integrated with the photosensitizer polyaniline (PANI) and the nitric oxide (NO) donor S-nitrosoglutathione (GSNO). The system enables mild photothermal therapy (MPTT)-NO synergy via NIR-triggered photothermal heating and controlled NO release. Under NIR irradiation, the generated mild heat induces AF cells to upregulate heat shock proteins (HSPs), thereby enhancing tissue repair. Furthermore, leveraging the thermosensitive release of NO from GSNO, PVA-CS-PANI-GSNO achieves spatiotemporal NO delivery under NIR control, which acts synergistically with MPTT to suppress inflammatory cytokine expression, promote ECM remodeling, and inhibit apoptosis of AF cells, ultimately facilitates the repair of the AF. By overcoming the limitations of systemic anti-inflammatory therapies imposed by the avascular nature of the AF, this strategy offers a promising avenue for the treatment of AF injuries associated with IVDD.
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