ReviewFrontiers in cellular neuroscience2014
Role of the kallikrein-kinin system in traumatic brain injury.
Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- The bradykinin B2 receptor as a context-dependent modulator of neural circuit function.Frontiers in cellular neuroscience · 2026Article
- Phenotypic similarity of adverse drug reactions and disease phenotypes is a bridge to mechanistic discovery.npj drug discovery · 2025Article
- Emerging trends and focus of research on the relationship between traumatic brain injury and gut microbiota: a visualized study.Frontiers in microbiology · 2023Review
- Modulation of Neuro-Inflammatory Signals in Microglia by Plasma Prekallikrein and Neuronal Cell Debris.Frontiers in pharmacology · 2021Article
- Association of Angiotensin-Converting Enzyme Inhibitors with Increased Mortality Among Patients with Isolated Severe Traumatic Brain Injury.Neurocritical care · 2019Article
- Human tissue kallikrein in the treatment of acute ischemic stroke.Therapeutic advances in neurological disorders · 2019Review
- Mechanisms of Global Cerebral Edema Formation in Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2017Review
- Alleviation of secondary brain injury, posttraumatic inflammation, and brain edema formation by inhibition of factor XIIa.Journal of neuroinflammation · 2017Article
- Transcriptome reveals the overexpression of a kallikrein gene cluster (KLK1/3/7/8/12) in the Tibetans with high altitude-associated polycythemia.International journal of molecular medicine · 2017Article
- Novel Innate Immune Genes Regulating the Macrophage Response to Gram Positive Bacteria.Genetics · 2016Article
- Demyelinating and thrombotic diseases of the central nervous system: common pathogenic and triggering factors.Frontiers in neurology · 2015Review
- Editorial: Mechanisms of neuroinflammation and inflammatory neurodegeneration in acute brain injury.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite improvements in acute intensive care, there are currently no specific therapies to ameliorate the effects of TBI. Successful therapeutic strategies for TBI should target multiple pathophysiologic mechanisms that occur at different stages of brain injury. The kallikrein-kinin system is a promising therapeutic target for TBI as it mediates key pathologic events of traumatic brain damage, such as edema formation, inflammation, and thrombosis. Selective and specific kinin receptor antagonists and inhibitors of plasma kallikrein and coagulation factor XII have been developed, and have already shown therapeutic efficacy in animal models of stroke and TBI. However, conflicting preclinical evaluation, as well as limited and inconclusive data from clinical trials in TBI, suggests that caution should be taken before transferring observations made in animals to humans. This review summarizes current evidence on the pathologic significance of the kallikrein-kinin system during TBI in animal models and, where available, the experimental findings are compared with human data.
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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.