ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Disrupting CSPG-Driven Microglia-Astrocyte Crosstalk Enables Scar-Free Repair in Spinal Cord Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed.
- Beyond Scar Removal: Reprogramming the Glial Scar for Neural Repair.International journal of molecular sciences · 2026Review
- Molecular Basis of Glia-ECM Interplay in Central Nervous System Homeostasis and Plasticity.Cells · 2026Review
- A four-dimensional spatial atlas of spinal cord injury reveals predominant Spp1-integrin signaling driving microglia-fibroblast crosstalk in fibrotic niches.Frontiers in immunology · 2026Article
- A pH-responsive and self-healing CEC/PEG-(CHO)Frontiers in neuroscience · 2026Article
- Disrupting CSPG-Driven Microglia-Astrocyte Crosstalk Enables Scar-Free Repair in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting glial scar formation for spinal cord injury: mechanisms, strategies, and research progress review.Frontiers in neuroscience · 2026Review
- Temporal dynamics of diffusion kurtosis imaging parallels astroglial GFAP expression in a non-traumatic spinal cord injury animal model of ischemia-reperfusion.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Glial scar formation represents a significant obstacle to neural regeneration following spinal cord injury (SCI), evolving from a protective glial response in the acute phase to a fibrotic and inhibitory barrier in the chronic stage. In this study, chondroitin sulphate proteoglycans (CSPGs) are identified as key regulators of scar maturation via a pathogenic microglia-astrocyte axis. CSPGs promote the transition of reactive astrocytes (RAs) into scar-forming astrocytes (SAs) by inducing a pro-inflammatory microglial phenotype. Mechanistically, CSPGs suppress cytochrome P450 (CYP450) enzyme activity in microglia, disrupting metabolic homeostasis and perpetuating inflammatory responses. Targeted degradation of CSPGs reprogrammes microglia toward an anti-inflammatory state, thereby attenuating SA differentiation and fibrotic matrix deposition. To enable spatiotemporally precise intervention, a reactive oxygen species-responsive, connective tissue growth factor-binding fusogenic lipopolyplex for RA-targeted delivery of the chondroitinase ABC (ChABC) gene is designed. This platform selectively degrades CSPGs at the lesion border, interrupts the maladaptive glial feedback loop, and facilitates scar-free repair after SCI. These findings reveal a metabolic mechanism underlying glial scarring and propose a precision nanotherapeutic strategy to modulate the SCI microenvironment, thereby enhancing neuronal regeneration and functional recovery.
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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 OpenQuestion graph.