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dECM scaffolds/ADSCs promote functional recovery after SCI. (A) BBB scores of different treatment groups of Control, SCI and dECM scaffolds/ADSCs at determined time after the operation. Data were presented as mean value ± SD. ***P < 0.001 compared with SCI group. (B) H&E and LFB staining results of spinal cord tissue in various groups. Scale bars = 75 μm.

dECM scaffolds/ADSCs promote functional recovery after SCI. (A) BBB scores of different treatment groups of Control, SCI and dECM scaffolds/ADSCs at determined time after the operation. Data were presented as mean value ± SD. ***P < 0.001 compared with SCI group. (B) H&E and LFB staining results of spinal cord tissue in various groups. Scale bars = 75 μm.

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Article
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Spinal cord injury (SCI) causes tissue destruction and neuronal apoptosis, which impede neural function recovery. Therefore, promoting neuronal regeneration and neural pathway reconstruction is crucial. In this study, a novel and facile decellularized extracellular matrix (dECM) scaffold seeded with adipose-derived stem cells (ADSCs) (dECM scaffold...

Citations

... ESCs [222], iPSCs [43,223], NSCs/NPCs [224,225], MSCs [180,181], OPCs [226], DPSCs [216] and ADSCs [227] Olfactory ensheathing cells [228] and Schwann cells [229] Microglia [230] Directly reprogrammed NPCs (drNPCs) [231][232][233] Gene therapies Nucleic acid-based therapies Delivery methods Other siRNA to AQP-4 [234], nNOS [235], iNOS [236], IL-6 [237], claudin-5 [238], RhoA [239,240], PLK-4 [241], PTEN [242,243], Sema3A [244], CTGF [245], combinatorial [246] and in combination with MSCs [242] Nanoparticle-coated siRNA [247][248][249], polymer nanocarriers [239], exosome delivery [243,245] extracellular vesicles [250], intrathecal delivery [240], photomechanical wave [251] and intranasal delivery [242] Chemogenetic stimulation [252] Biomaterials Porous polymers Natural polymers Nanoscaffolds Nerve guidance Other Hydrogels [180,181,253,254], PLGA [255] and PLA [256] Collagen [181,257], CS [258], silk [259,260], decellularised ECM [227], modified gelatine [261] R-GSIK [262], electrospun nanofiber nets [263] and gene scaffolds [264] Gold nanoparticle nerve guidance conduits [265] and collagen conduits [266] Graphene oxide [267], IGF-1 delivery via nanofibrous dural substitutes [197] and ROS scavenger materials [170,171] [268,269], magnetic [270,271], ultrasound [272,273], light (photobiomodulation) [274,275] and combinatorial [276] Spinal stimulators [277] in combination with task training [278] Exoskeletons [279,280] and neuroprosthesis [281] ...
... ESCs [222], iPSCs [43,223], NSCs/NPCs [224,225], MSCs [180,181], OPCs [226], DPSCs [216] and ADSCs [227] Olfactory ensheathing cells [228] and Schwann cells [229] Microglia [230] Directly reprogrammed NPCs (drNPCs) [231][232][233] Gene therapies Nucleic acid-based therapies Delivery methods Other siRNA to AQP-4 [234], nNOS [235], iNOS [236], IL-6 [237], claudin-5 [238], RhoA [239,240], PLK-4 [241], PTEN [242,243], Sema3A [244], CTGF [245], combinatorial [246] and in combination with MSCs [242] Nanoparticle-coated siRNA [247][248][249], polymer nanocarriers [239], exosome delivery [243,245] extracellular vesicles [250], intrathecal delivery [240], photomechanical wave [251] and intranasal delivery [242] Chemogenetic stimulation [252] Biomaterials Porous polymers Natural polymers Nanoscaffolds Nerve guidance Other Hydrogels [180,181,253,254], PLGA [255] and PLA [256] Collagen [181,257], CS [258], silk [259,260], decellularised ECM [227], modified gelatine [261] R-GSIK [262], electrospun nanofiber nets [263] and gene scaffolds [264] Gold nanoparticle nerve guidance conduits [265] and collagen conduits [266] Graphene oxide [267], IGF-1 delivery via nanofibrous dural substitutes [197] and ROS scavenger materials [170,171] [268,269], magnetic [270,271], ultrasound [272,273], light (photobiomodulation) [274,275] and combinatorial [276] Spinal stimulators [277] in combination with task training [278] Exoskeletons [279,280] and neuroprosthesis [281] ...
Article
Full-text available
Traumatic injury to the brain and spinal cord (neurotrauma) is a common event across populations and often causes profound and irreversible disability. Pathophysiological responses to trauma exacerbate the damage of an index injury, propagating the loss of function that the central nervous system (CNS) cannot repair after the initial event is resolved. The way in which function is lost after injury is the consequence of a complex array of mechanisms that continue in the chronic phase post-injury to prevent effective neural repair. This review summarises the events after traumatic brain injury (TBI) and spinal cord injury (SCI), comprising a description of current clinical management strategies, a summary of known cellular and molecular mechanisms of secondary damage and their role in the prevention of repair. A discussion of current and emerging approaches to promote neuroregeneration after CNS injury is presented. The barriers to promoting repair after neurotrauma are across pathways and cell types and occur on a molecular and system level. This presents a challenge to traditional molecular pharmacological approaches to targeting single molecular pathways. It is suggested that novel approaches targeting multiple mechanisms or using combinatorial therapies may yield the sought-after recovery for future patients.