ArticleThe Journal of biological chemistry2012
Targeted gene inactivation of calpain-1 suppresses cortical degeneration due to traumatic brain injury and neuronal apoptosis induced by oxidative stress.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- A 3D Human Neuron-on-Chip Platform to Monitor Neuronal Injury Responses.Advanced healthcare materials · 2026Article
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Inhibition of calpain-mediated HMGB1 alleviates cardiac inflammation and dysfunction induced by ultra-processed foods.JCI insight · 2026Article
- Ubiquitous calpastatin overexpression in brain-injured mice attenuates motor and cognitive behavioral deficits without overt neuroprotection.Molecular and cellular neurosciences · 2025Article
- Oxytocin Anti-Apoptotic Potential Mediates Neuroprotection Against 3-Nitropropionic Acid-Induced Huntington's Disease-Like Pathophysiology in Rats: Involvement of Calpain-2/p25 Cdk5/MEF-2 Signaling Pathway.Neurochemical research · 2025Article
- Calpain: the regulatory point of myocardial ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2023Review
- Endoplasmic reticulum stress-related secretory proteins as biomarkers of early myocardial ischemia-induced sudden cardiac deaths.International journal of legal medicine · 2022Article
- Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway.Neural plasticity · 2022Article
- Local delivery of RhoA siRNA by PgP nanocarrier reduces inflammatory response and improves neuronal cell survival in a rat TBI model.Nanomedicine : nanotechnology, biology, and medicine · 2021Article
- Knockout of calpain-1 protects against high-fat diet-induced liver dysfunction in mouse through inhibiting oxidative stress and inflammation.Food science & nutrition · 2021Article
- Glia Maturation Factor (GMF) Regulates Microglial Expression Phenotypes and the Associated Neurological Deficits in a Mouse Model of Traumatic Brain Injury.Molecular neurobiology · 2020Article
- Calpain-1 ablation partially rescues disease-associated hallmarks in models of Machado-Joseph disease.Human molecular genetics · 2020Article
- Endoplasmic reticulum stress-induced complex I defect: Central role of calcium overload.Archives of biochemistry and biophysics · 2020Article
- Cell Death and Recovery in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
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- Paricalcitol accelerates BACE1 lysosomal degradation and inhibits calpain-1 dependent neuronal loss in APP/PS1 transgenic mice.EBioMedicine · 2019Article
- Suppressing the NaCell death & disease · 2019Article
- Gene Profiling of Nucleus Basalis Tau Containing Neurons in Chronic Traumatic Encephalopathy: A Chronic Effects of Neurotrauma Consortium Study.Journal of neurotrauma · 2018Article
- Neuronal Cell Death.Physiological reviews · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Calpains are calcium-regulated cysteine proteases that have been implicated in the regulation of cell death pathways. Here, we used our calpain-1 null mouse model to evaluate the function of calpain-1 in neural degeneration following a rodent model of traumatic brain injury. In vivo, calpain-1 null mice show significantly less neural degeneration and apoptosis and a smaller contusion 3 days post-injury than wild type littermates. Protection from traumatic brain injury corroborated with the resistance of calpain-1 neurons to apoptosis induced by oxidative stress. Biochemical analysis revealed that caspase-3 activation, extracellular calcium entry, mitochondrial membrane permeability, and release of apoptosis-inducing factor from mitochondria are partially blocked in the calpain-1 null neurons. These findings suggest that the calpain-1 knock-out mice may serve as a useful model system for neuronal protection and apoptosis in traumatic brain injury and other neurodegenerative disorders in which oxidative stress plays a role.
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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.