ArticleThe American journal of pathology2010
The alternative and terminal pathways of complement mediate post-traumatic spinal cord inflammation and injury.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- APOE-mediated lipid transport prevents C1q-related synaptic loss after spinal cord injury via attenuating macrophage lipid stress.Journal of neuroinflammation · 2026Article
- Immune Activation Following Spinal Cord Injury: A Review Focused on Inflammatory Changes in the Spinal Cord.International journal of molecular sciences · 2025Review
- Exploring Structural and Molecular Features of Sciatic Nerve Lesions in Diabetic Neuropathy: Unveiling Pathogenic Pathways and Targets.Diabetes · 2025Article
- The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024Review
- Photobiomodulation provides neuroprotection through regulating mitochondrial fission imbalance in the subacute phase of spinal cord injury.Neural regeneration research · 2023Article
- Assessing the Global Impact on the Mouse Kidney After Traumatic Brain Injury: A Transcriptomic Study.Journal of inflammation research · 2022Article
- Complement C6 deficiency exacerbates pathophysiology after spinal cord injury.Scientific reports · 2020Article
- Therapeutic Effects of Minocycline Pretreatment in the Locomotor and Sensory Complications of Spinal Cord Injury in an Animal Model.Journal of molecular neuroscience : MN · 2020Article
- Mitochondrial biogenesis as a therapeutic target for traumatic and neurodegenerative CNS diseases.Experimental neurology · 2020Review
- European Society for Immunodeficiencies (ESID) and European Reference Network on Rare Primary Immunodeficiency, Autoinflammatory and Autoimmune Diseases (ERN RITA) Complement Guideline: Deficiencies, Diagnosis, and Management.Journal of clinical immunology · 2020Article
- An "Outside-In" and "Inside-Out" Consideration of Complement in the Multiple Sclerosis Brain: Lessons From Development and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
- RNA sequencing screening of differentially expressed genes after spinal cord injury.Neural regeneration research · 2019Article
- A Causal Relationship in Spinal Cord Injury Rat Model Between Microglia Activation and EGFR/MAPK Detected by Overexpression of MicroRNA-325-3p.Journal of molecular neuroscience : MN · 2019Article
- Complement receptor C3aR1 controls neutrophil mobilization following spinal cord injury through physiological antagonism of CXCR2.JCI insight · 2019Article
- Ursodeoxycholic Acid Inhibits Inflammatory Responses and Promotes Functional Recovery After Spinal Cord Injury in Rats.Molecular neurobiology · 2019Article
- Article
- Exosomes Derived From Bone Marrow Mesenchymal Stem Cells Inhibit Complement Activation In Rats With Spinal Cord Injury.Drug design, development and therapy · 2019Article
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System.Frontiers in immunology · 2019Review
- Anti-inflammatory effects of Metformin improve the neuropathic pain and locomotor activity in spinal cord injured rats: introduction of an alternative therapy.Spinal cord · 2018Article
- The role of the complement system in traumatic brain injury: a review.Journal of neuroinflammation · 2018Review
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7 authors at 5 institutions in 3 countries.
Funding
Abstract
Complement is implicated in the inflammatory response and the secondary neuronal damage that occurs after traumatic spinal cord injury (SCI). Complement can be activated by the classical, lectin, or alternative pathways, all of which share a common terminal pathway that culminates in formation of the cytolytic membrane attack complex (MAC). Here, we investigated the role of the alternative and terminal complement pathways in SCI. Mice deficient in the alternative pathway protein factor B (fB) were protected from traumatic SCI in terms of reduced tissue damage and demyelination, reduced inflammatory cell infiltrate, and improved functional recovery. In a clinically relevant paradigm, treatment of mice with an anti-fB mAb resulted in similarly improved outcomes. These improvements were associated with decreased C3 and fB deposition. On the other hand, deficiency of CD59, an inhibitor of the membrane attack complex, resulted in significantly increased injury and impaired functional recovery compared to wild-type mice. Increased injury in CD59-deficient mice was associated with increased MAC deposition, while levels of C3 and fB were unaffected. These data indicate key roles for the alternative and terminal complement pathways in the pathophysiology of SCI. Considering a previous study demonstrating an important role for the classical pathway in promoting SCI, it is likely that the alternative pathway plays a critical role in amplifying classical pathway initiated complement activation.
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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.