ReviewCells2020
Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- How muscle talks to brain: apelin protein mediates exercise-induced antidepressant effects.Molecular psychiatry · 2026Article
- Quantitative Characterization of Innate and Adaptive Pharmacology of Allogeneic anti-CD20 Chimeric Antigen Receptor (CAR) Vδ1 γδ T cells using Multiscale Mechanistic Modeling.The AAPS journal · 2026Article
- γδ T Cell-Mediated Neuroimmune Interactions in Skin Inflammation and Allergy.Clinical reviews in allergy & immunology · 2026Review
- A small-molecule stabilizer of the calpastatin-calpain-2 complex restores mitochondrial function and mitigates neurodegeneration.Science advances · 2026Article
- A Bioinformatics Analysis on the Subtypes of Hepatocellular Carcinoma Related to RNA Processing Genes to Reveal Prognosis and Immune Microenvironment Features.Digestive diseases and sciences · 2025Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Subtype-specific divergent roles of calpain-1 and calpain-2 in basal A triple-negative breast cancer.BMC molecular and cell biology · 2025Article
- Ischemic stroke and intervention strategies based on the timeline of stroke progression: Review and prospects.Acta pharmaceutica Sinica. B · 2025Review
- Ubiquitous calpastatin overexpression in brain-injured mice attenuates motor and cognitive behavioral deficits without overt neuroprotection.Molecular and cellular neurosciences · 2025Article
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- Single-cell protein production from photosynthetic bacteria wastewater treatment.Biotechnology letters · 2025Review
- The impact of chronic intermittent hypoxia on enzymatic activity in memory-associated brain regions of male and female rats.Biology of sex differences · 2025Article
- Terpinen-4-ol suppresses proliferation and motility of cutaneous squamous cell carcinoma cells by enhancing calpain-2 expression.Oncology research · 2025Article
- Cell death in acute lung injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis.Frontiers in pharmacology · 2025Review
- The impact of chronic intermittent hypoxia on enzymatic activity in memory-associated brain regions of male and female rats.Research square · 2024Article
- Autophagy modulators in type 2 diabetes: A new perspective.Journal of diabetes · 2024Review
- Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calpains are a family of soluble calcium-dependent proteases that are involved in multiple regulatory pathways. Our laboratory has focused on the understanding of the functions of two ubiquitous calpain isoforms, calpain-1 and calpain-2, in the brain. Results obtained over the last 30 years led to the remarkable conclusion that these two calpain isoforms exhibit opposite functions in the brain. Calpain-1 activation is required for certain forms of synaptic plasticity and corresponding types of learning and memory, while calpain-2 activation limits the extent of plasticity and learning. Calpain-1 is neuroprotective both during postnatal development and in adulthood, while calpain-2 is neurodegenerative. Several key protein targets participating in these opposite functions have been identified and linked to known pathways involved in synaptic plasticity and neuroprotection/neurodegeneration. We have proposed the hypothesis that the existence of different PDZ (PSD-95, DLG and ZO-1) binding domains in the C-terminal of calpain-1 and calpain-2 is responsible for their association with different signaling pathways and thereby their different functions. Results with calpain-2 knock-out mice or with mice treated with a selective calpain-2 inhibitor indicate that calpain-2 is a potential therapeutic target in various forms of neurodegeneration, including traumatic brain injury and repeated concussions.
Indexed as
Identifiers
What OpenQuestion holds
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.