ReviewMaterials today. Bio2026
Reprogramming the oxidative microenvironment: Antioxidant nanoplatforms for central nervous system repair.
Review 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
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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.
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
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute central nervous system (CNS) injuries-such as ischemic stroke, traumatic brain injury (TBI), and spinal cord injury (SCI)-trigger a severe, self-reinforcing oxidative microenvironment. This reactive oxygen species (ROS)-driven cascade accelerates secondary injury mechanisms, including sustained neuroinflammation, blood-brain and blood-spinal cord barrier (BBB/BSCB) disruption, and irreversible mitochondrial dysfunction, ultimately forming a hostile niche that impedes spontaneous neural repair. While current clinical modalities address the primary physical or ischemic insults, they largely fail to mitigate this persistent oxidative stress. Furthermore, conventional small-molecule antioxidants are severely limited by poor pharmacokinetic profiles, inefficient barrier penetration, and an inability to provide spatiotemporally controlled ROS scavenging. To overcome these therapeutic bottlenecks, advanced antioxidant nanoplatforms have emerged as active regulators of the injury milieu. This review comprehensively examines the design principles of next-generation nanotherapeutics, highlighting strategies such as receptor-mediated transcytosis for active barrier traversal, stimuli-responsive mechanisms for on-site activation, and the integration of multi-catalytic inorganic nanozymes for subcellular precision. Beyond stoichiometric ROS scavenging, these platforms facilitate precise redox modulation that reprograms cellular fate. We detail how restoring redox homeostasis promotes the crucial M1-to-M2 polarization of microglia/macrophages, preserves mitochondrial integrity against apoptotic cascades, and creates a permissive microenvironment conducive to axonal regeneration and remyelination across stroke, TBI, and SCI models. Finally, we outline the critical translational challenges that must be addressed to transition these nanoplatforms into clinical practice, emphasizing the need for long-term biodistribution and immunotoxicity profiling, refined pharmacokinetic/pharmacodynamic (PK/PD) modeling, and the establishment of scalable, Good Manufacturing Practice (GMP)-compatible protocols.
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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.