ReviewTrends in molecular medicine2010
Mechanisms of axonal injury: internodal nanocomplexes and calcium deregulation.
Review in Trends in molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 156 citations in OpenAlex.
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Extrinsic Regulation of Optic Nerve Axon Regeneration in the Adult Central Nervous System.Cells · 2026Review
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Combined treatment targeting Ca2+ store mediated Ca2+ release and store-operated calcium entry reduces secondary axonal degeneration and improves functional outcome after SCI.Experimental neurology · 2025Article
- Article
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- Neural regeneration in the human central nervous system-from understanding the underlying mechanisms to developing treatments. Where do we stand today?Frontiers in neurology · 2024Review
- CaNeural regeneration research · 2023Article
- Cyclophilin D-induced mitochondrial impairment confers axonal injury after intracerebral hemorrhage in mice.Neural regeneration research · 2023Article
- Potential physiological and pathological roles for axonal ryanodine receptors.Neural regeneration research · 2023Review
- Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023Review
- Relationship between Hypoxic and Immune Pathways Activation in the Progression of Neuroinflammation: Role of HIF-1α and Th17 Cells.International journal of molecular sciences · 2023Review
- Retinal ganglion cells adapt to ionic stress in experimental glaucoma.Frontiers in neuroscience · 2023Article
- A new form of axonal pathology in a spinal model of neuromyelitis optica.Brain : a journal of neurology · 2022Article
- Inhibiting Calcium Release from Ryanodine Receptors Protects Axons after Spinal Cord Injury.Journal of neurotrauma · 2022Article
- Direct Ryanodine Receptor-2 Knockout in Primary Afferent Fibers Modestly Affects Neurological Recovery after Contusive Spinal Cord Injury.Neurotrauma reports · 2022Article
- Axonal spheroids in neurodegeneration.Molecular and cellular neurosciences · 2021Review
- Adaptive responses to neurodegenerative stress in glaucoma.Progress in retinal and eye research · 2021Review
- Loss of the K+ channel Kv2.1 greatly reduces outward dark current and causes ionic dysregulation and degeneration in rod photoreceptors.The Journal of general physiology · 2021Article
- Neuron-Oligodendrocyte Interactions in the Structure and Integrity of Axons.Frontiers in cell and developmental biology · 2021Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Axonal degeneration causes morbidity in many neurological conditions including stroke, neurotrauma and multiple sclerosis. The limited ability of central nervous system (CNS) neurons to regenerate, combined with the observation that axonal damage causes clinical disability, has spurred efforts to investigate the mechanisms of axonal degeneration. Ca influx from outside the axon is a key mediator of injury. More recently, substantial pools of intra-axonal Ca sequestered in the 'axoplasmic reticulum' have been reported. These Ca stores are under the control of multimolecular 'nanocomplexes' located along the internodes under the myelin. The overactivation of these complexes during disease can lead to a lethal release of Ca from intra-axonal stores. Rich receptor pharmacology offers tantalizing therapeutic options targeting these nanocomplexes in the many diseases where axonal degeneration is prominent.
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.