ArticlePloS one2013
Selective inhibition of matrix metalloproteinase-9 attenuates secondary damage resulting from severe traumatic brain injury.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Association of cerebrospinal fluid protein biomarkers with outcomes in patients with traumatic and non-traumatic acute brain injury: systematic review of the literature.Critical care (London, England) · 2021Pooled it
- The Profile of MMP-9, MMP-9 mRNA Expression, -1562 C/T Polymorphism and Outcome in High-risk Traumatic Brain Injury: The Effect of Therapeutic Mild Hypothermia.Neurologia medico-chirurgica · 2017Trial
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal of neuroinflammation · 2026Article
- Decoding spontaneous intracerebral hemorrhage: mechanistic breakthroughs and disruptive revolution in pharmacological treatment.Experimental & molecular medicine · 2026Review
- Neuronal Toll-like Receptor-4 regulation of Matrix Metalloproteinase-9 Activity Mediates Dentate Circuit Dysfunction after Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Matrix Metalloproteinases in Glioma: Drivers of Invasion and Therapeutic Targets.Biotech (Basel (Switzerland)) · 2025Review
- Ring Opening Functionalization of Thiolactone Homopolymers for ROS Scavenging.Journal of polymer science (2020) · 2024Article
- Developmental Regulation of Matrix Metalloproteinases in Response to Multifactorial, Severe Traumatic Brain Injuries during Immaturity.Developmental neuroscience · 2024Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Gelatin Zymography Can Be Performed on Fixed Brain Tissue.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- Article
- Matrix metalloproteinase profiling and their roles in disease.RSC advances · 2023Review
- The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome.Frontiers in immunology · 2023Review
- Theranostic Copolymers Neutralize Reactive Oxygen Species and Lipid Peroxidation Products for the Combined Treatment of Traumatic Brain Injury.Biomacromolecules · 2022Article
- Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach.Neurochemistry international · 2021Review
- Pathophysiological Responses and Roles of Astrocytes in Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- MMP9 modulation improves specific neurobehavioral deficits in a mouse model of Alzheimer's disease.BMC neuroscience · 2021Article
- The emerging role of neutrophils as modifiers of recovery after traumatic injury to the developing brain.Experimental neurology · 2019Review
- Matrix Metalloproteinase 9 and Osteopontin Interact to Support Synaptogenesis in the Olfactory Bulb after Mild Traumatic Brain Injury.Journal of neurotrauma · 2019Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a leading cause of death and long-term disability. Following the initial insult, severe TBI progresses to a secondary injury phase associated with biochemical and cellular changes. The secondary injury is thought to be responsible for the development of many of the neurological deficits observed after TBI and also provides a window of opportunity for therapeutic intervention. Matrix metalloproteinase-9 (MMP-9 or gelatinase B) expression is elevated in neurological diseases and its activation is an important factor in detrimental outcomes including excitotoxicity, mitochondrial dysfunction and apoptosis, and increases in inflammatory responses and astrogliosis. In this study, we used an experimental mouse model of TBI to examine the role of MMP-9 and the therapeutic potential of SB-3CT, a mechanism-based gelatinase selective inhibitor, in ameliorating the secondary injury. We observed that activation of MMP-9 occurred within one day following TBI, and remained elevated for 7 days after the initial insult. SB-3CT effectively attenuated MMP-9 activity, reduced brain lesion volumes and prevented neuronal loss and dendritic degeneration. Pharmacokinetic studies revealed that SB-3CT and its active metabolite, p-OH SB-3CT, were rapidly absorbed and distributed to the brain. Moreover, SB-3CT treatment mitigated microglial activation and astrogliosis after TBI. Importantly, SB-3CT treatment improved long-term neurobehavioral outcomes, including sensorimotor function, and hippocampus-associated spatial learning and memory. These results demonstrate that MMP-9 is a key target for therapy to attenuate secondary injury cascades and that this class of mechanism-based gelatinase inhibitor-with such desirable pharmacokinetic properties-holds considerable promise as a potential pharmacological treatment of TBI.
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Registered trials
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.