ArticleJournal of neurotrauma2018
Protection against TBI-Induced Neuronal Death with Post-Treatment with a Selective Calpain-2 Inhibitor in Mice.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Calpain Inhibitors as Potential Therapeutic Modulators in Neurodegenerative Diseases.Neurochemical research · 2022Pooled it
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Ubiquitous calpastatin overexpression in brain-injured mice attenuates motor and cognitive behavioral deficits without overt neuroprotection.Molecular and cellular neurosciences · 2025Article
- Review
- Review
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- Spatial Measurement and Inhibition of Calpain Activity in Traumatic Brain Injury with an Activity-Based Nanotheranostic Platform.ACS nano · 2024Article
- Trauma in Neonatal Acute Brain Slices Alters Calcium and Network Dynamics and Causes Calpain-Mediated Cell Death.eNeuro · 2024Article
- Identification and neuroprotective properties of NA-184, a calpain-2 inhibitor.Pharmacology research & perspectives · 2024Article
- Electrolyte Imbalance and Neurologic Injury.CNS & neurological disorders drug targets · 2024Review
- Revisiting the calpain hypothesis of learning and memory 40 years later.Frontiers in molecular neuroscience · 2024Review
- Calpain-2 Inhibitors as Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Nicotinamide Mononucleotide Adenylyl Transferase 2 Inhibition Aggravates Neurological Damage after Traumatic Brain Injury in a Rat Model.Journal of Korean Neurosurgical Society · 2023Article
- Inhibition of Calpain Attenuates Degeneration of Substantia Nigra Neurons in the Rotenone Rat Model of Parkinson's Disease.International journal of molecular sciences · 2022Article
- Combined cell grafting and VPA administration facilitates neural repair through axonal regeneration and synaptogenesis in traumatic brain injury.Acta biochimica et biophysica Sinica · 2022Article
- Hyperacute Excitotoxic Mechanisms and Synaptic Dysfunction Involved in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2022Review
- Protective Effects of Aquaporin-4 Deficiency on Longer-term Neurological Outcomes in a Mouse Model.Neurochemical research · 2021Article
- A systemic immune challenge to model hospital-acquired infections independently regulates immune responses after pediatric traumatic brain injury.Journal of neuroinflammation · 2021Article
- The Spread of Spectrin in Ataxia and Neurodegenerative Disease.Journal of experimental neurology · 2021Article
- Changes in neurodegeneration-related miRNAs in brains from CAPN1BBA advances · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic Brain Injury (TBI) is a major cause of death and disability worldwide. The calcium-dependent protease, calpain, has been shown to be involved in TBI-induced neuronal death. However, whereas various calpain inhibitors have been tested in several animal models of TBI, there has not been any clinical trial testing the efficacy of calpain inhibitors in human TBI. One important reason for this could be the lack of knowledge regarding the differential functions of the two major calpain isoforms in the brain, calpain-1 and calpain-2. In this study, we used the controlled cortical impact (CCI) model in mice to test the roles of calpain-1 and calpain-2 in TBI-induced neuronal death. Immunohistochemistry (IHC) with calpain activity markers performed at different time-points after CCI in wild-type and calpain-1 knock-out (KO) mice showed that calpain-1 was activated early in cortical areas surrounding the impact, within 0-8 h after CCI, whereas calpain-2 activation was delayed and was predominant during 8-72 h after CCI. Calpain-1 KO enhanced cell death, whereas calpain-2 activity correlated with the extent of cell death, suggesting that calpain-1 activation suppresses and calpain-2 activation promotes cell death following TBI. Systemic injection(s) of a calpain-2 selective inhibitor, NA101, at 1 h or 4 h after CCI significantly reduced calpain-2 activity and cell death around the impact site, reduced the lesion volume, and promoted motor and learning function recovery after TBI. Our data indicate that calpain-1 activity is neuroprotective and calpain-2 activity is neurodegenerative after TBI, and that a selective calpain-2 inhibitor can reduce TBI-induced cell death.
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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.