ArticleBioactive materials2025
Novel carbon dots with dual Modulatory effects on the bone marrow and spleen as a potential therapeutic candidate for treating spinal cord injury.
Article in Bioactive materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neonatal small extracellular vesicle-loaded GelNB hydrogel reprograms the vascular-immune microenvironment for spinal cord injury repair.Bioactive materials · 2026Article
- Biomaterial-Based Emergency Intervention for Secondary Spinal Cord Injury.Small science · 2025Review
- Carbon dots derived from Ligusticum Chuanxiong mitigate cardiac injury by disrupting the harmful oxidative stress-apoptosis cycle.Journal of nanobiotechnology · 2025Article
- Exosomes: a promising microenvironment modulator for spinal cord injury treatment.International journal of biological sciences · 2025Review
- Antioxidant nanozymes: current status and future perspectives in spinal cord injury treatments.Theranostics · 2025Review
Corrections and comments
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Authors and funding
20 authors.
Funding
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Abstract
Spinal cord injury triggers leukocyte mobilization from the peripheral circulation to the injury site, exacerbating spinal cord damage. Simultaneously, bone marrow hematopoietic stem cells (HSCs) and splenic leukocytes rapidly mobilize to replenish the depleted peripheral blood leukocyte pool. However, current treatments for spinal cord injuries overlook interventions targeting peripheral immune organs and tissues, highlighting the need to develop novel drugs capable of effectively regulating peripheral immunity and treating spinal cord injuries. In this study, we designed, synthesized, and characterized novel Ejiao carbon dots (EJCDs) that inhibit myeloid cell proliferation and peripheral migration by promoting HSC self-renewal, and distinct differentiation into erythroid progenitors in vitro and in vivo. Additionally, EJCDs attenuate the immune response in the spleen, leukocytes' reservoir, following spinal cord injury by diminishing the local infiltration of monocytes and macrophages while promoting motor function recovery. These effects are mediated through the downregulation of CCAAT enhancer binding protein-β expression in the spleen and the upregulation of FZD4 protein expression in Lin
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