ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
A Dual-Functional Nanoplatform Targeting the dsDNA-cGAS Axis to Mitigate Disc Degeneration and Aberrant Innervation.
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. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
Pathological sensory nerve ingrowth into degenerated intervertebral discs contributes to discogenic pain, yet strategies that concurrently mitigate disc degeneration and pathological innervation remain limited. Here, we found that senescent nucleus pulposus (NP) cells accumulated and released double-stranded DNA (dsDNA), which reinforced NP cell senescence and matrix catabolism. The accumulated dsDNA also activated cGAS-STING signaling, increased Netrin-1 expression, and promoted neuronal migration and neurite outgrowth. Guided by these findings, we developed RU@PEI-ZIF, a dual-functional nanoplatform combining PEI-mediated dsDNA scavenging with ZIF-8-mediated delivery of the cGAS inhibitor RU.521. RU@PEI-ZIF displayed dsDNA-binding capacity, cytocompatibility, and pH-responsive RU.521 release. In senescent NP cells, RU@PEI-ZIF reduced extracellular and cytosolic dsDNA, attenuated cGAS-STING-associated inflammatory and neurotrophic signaling, and reduced NP cell-mediated neuronal migration and neurite outgrowth. In an animal model of disc degeneration, intradiscal RU@PEI-ZIF reduced disc degeneration, NP cell senescence, pathological sensory innervation, and pain hypersensitivity. These findings support RU@PEI-ZIF as a dual-action nanotherapeutic strategy targeting both disc degeneration and pathological innervation.
Indexed as
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.