ArticleThe Journal of pharmacology and experimental therapeutics2012
Effect of fasudil, a selective inhibitor of Rho kinase activity, in the secondary injury associated with the experimental model of spinal cord trauma.
Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- The potential role of RhoA/ROCK-inhibition on locomotor recovery after spinal cord injury: a systematic review of in-vivo studies.Spinal cord · 2025Pooled it
- Augmentation of functional recovery viaJournal of orthopaedic translation · 2024Article
- Microglia in depression: an overview of microglia in the pathogenesis and treatment of depression.Journal of neuroinflammation · 2022Review
- Inflammation after spinal cord injury: a review of the critical timeline of signaling cues and cellular infiltration.Journal of neuroinflammation · 2021Review
- Article
- Role of Smad3 inhibitor and the pyroptosis pathway in spinal cord injury.Experimental and therapeutic medicine · 2020Article
- Fasudil may induce the differentiation of bone marrow mesenchymal stem cells into neuron‑like cells via the Wnt/β‑catenin pathway.Molecular medicine reports · 2019Article
- Potential immunotherapies for traumatic brain and spinal cord injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Review
- Perturbing chondroitin sulfate proteoglycan signaling through LAR and PTPσ receptors promotes a beneficial inflammatory response following spinal cord injury.Journal of neuroinflammation · 2018Article
- Programmed Cell Death after Intracerebral Hemorrhage.Current neuropharmacology · 2018Review
- Role of Caspase-8 and Fas in Cell Death After Spinal Cord Injury.Frontiers in molecular neuroscience · 2018Review
- RhoA knockdown by cationic amphiphilic copolymer/siRhoA polyplexes enhances axonal regeneration in rat spinal cord injury model.Biomaterials · 2017Article
- Role of Rho Kinase Inhibition in the Protective Effect of Fasudil and Simvastatin Against 3-Nitropropionic Acid-Induced Striatal Neurodegeneration and Mitochondrial Dysfunction in Rats.Molecular neurobiology · 2016Article
- Activation and Regulation of NLRP3 Inflammasome by Intrathecal Application of SDF-1a in a Spinal Cord Injury Model.Molecular neurobiology · 2016Article
- RhoA/Rho kinase in spinal cord injury.Neural regeneration research · 2016Article
- Therapeutic Hypothermia in Spinal Cord Injury: The Status of Its Use and Open Questions.International journal of molecular sciences · 2015Review
- Rho family GTPases: key players in neuronal development, neuronal survival, and neurodegeneration.Frontiers in cellular neuroscience · 2014Review
- Rho kinase: A new target for treatment of cerebral ischemia/reperfusion injury.Neural regeneration research · 2013Article
- The role of pharmacotherapy in modifying the neurological status of patients with spinal and spinal cord injuries.Revista brasileira de ortopediaReview
Corrections and comments
- Expression of concern
- Expression of concern
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho kinase (ROK) may play an important role in regulating the biological events of cells, including proliferation, differentiation, and survival/death. Blockade of ROK promotes axonal regeneration and neuron survival in vivo and in vitro, thereby exhibiting potential clinical applications in spinal cord damage and stroke. The aim of this experimental study was to determine the role of ROK signaling pathways in the inflammatory response, in particular in the secondary injury associated with the experimental model of spinal cord trauma. The injury was induced by application of vascular clips to the dura via a four-level T5 to T8 laminectomy in mice. Fasudil was administered in mice (10 mg/kg i.p.) 1 and 6 h after the trauma. The treatment with fasudil significantly decreased 1) histological damage; 2) motor recovery; 3) nuclear factor-κB (NF-κB) expression; 4) ROK activity; 5) inflammasome activation (caspase-1 and NOD-like receptor family, pyrin domain-containing 3 expression); 6) production of proinflammatory cytokine such as tumor necrosis factor and interleukin-1β (IL-1β); 7) neutrophil infiltration; 8) nitrotyrosine and poly-ADP-ribose formation; 9) glial fibrillary acidic protein expression; 10) apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, FAS ligand expression, and Bax and Bcl-2 expression); and 11) mitogen-activated protein kinase activation (phospho-extracellular signal-regulated kinase and phospho-c-Jun NH(2)-terminal kinase expression). Our results indicate that inhibition of ROK by fasudil may represent a useful therapeutic perspective in the treatment of inflammation associated with spinal cord trauma.
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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 OpenQuestion graph.