ArticleMaterials today. Bio2026
A lesion-responsive ZIF-8/zinc-myricetin nano-biointerface remodels mitochondrial-immune crosstalk for spinal cord repair.
Article in Materials today. Bio, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) creates a hostile lesion microenvironment characterized by oxidative stress, mitochondrial dysfunction, inflammatory metabolic remodeling, and pyroptotic cell death, which collectively restrict neural repair. Here, we engineered a lesion-responsive ZIF-8/zinc-myricetin nano-biointerface, AST@ZIF-8@Zn-MYR, to coordinate redox regulation, mitochondrial protection, and immune microenvironment remodeling after SCI. Astaxanthin was encapsulated within a ZIF-8 core to improve cargo protection and enable pH/ROS-responsive release, while a zinc-myricetin coordination shell was constructed as a redox-active interfacial layer. The resulting nanoplatform exhibited a well-dispersed core-shell structure, responsive release behavior, broad-spectrum ROS-scavenging activity, and favorable cytocompatibility. In activated microglia, AST@ZIF-8@Zn-MYR reduced intracellular and mitochondrial oxidative stress, restored mitochondrial bioenergetics, alleviated glycolysis-biased immunometabolic remodeling, and attenuated inflammatory activation together with NLRP3/GSDMD-associated molecular signaling linked to pyroptosis. In oxidatively injured neuronal cells, the nano-biointerface preserved mitochondrial membrane potential, improved respiratory function, rebalanced mitochondrial dynamics, and supported neuronal survival and neurite outgrowth. In a rat SCI model, local administration attenuated acute oxidative-inflammatory injury, improved lesion microenvironment remodeling, preserved axon-myelin structures, and was associated with improved electrophysiological and locomotor outcomes. These findings identify AST@ZIF-8@Zn-MYR as a responsive bioactive nanomaterial that bridges interfacial redox chemistry and mitochondrial-immune regulation for spinal cord repair.
Indexed as
Identifiers
What Socratic 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 Socratic graph.