ReviewNeurobiology of disease2021
Mechanosensation in traumatic brain injury.
Review in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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.
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Who cites it
59 citing papers in PubMed, 89 citations in OpenAlex.
- Assessing Motion Fidelity During Closed-Head Rotational Acceleration Traumatic Brain Injury in Pigs.Research square · 2026Article
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- Article
- Auditory Stimulation of Slow-Wave Sleep Promotes Recovery after Brain Injury in an Animal Model.Annals of neurology · 2026Article
- Calcium-Dependent Cytoskeletal Collapse and Recovery of Axons After Partial Laser Ablation.Journal of neurochemistry · 2026Article
- Focused ultrasound-induced cavitation in a human brain microphysiological system produces injury signaling biomarkers consistent with blast trauma.npj biomedical innovations · 2026Article
- Mechanisms of inflammatory response in secondary brain injury: a review of computational approaches, challenges, and future directions.Biomechanics and modeling in mechanobiology · 2026Review
- Mechanical Stretch Disrupts Calcium Dynamics and Redistributes Piezo1 in Human Astrocytes.Annals of biomedical engineering · 2026Article
- Development and Evaluation of "a PEGylated Anti-Tau ScFv for SPECT Imaging" in a Rat Model of Traumatic Brain Injury.Pharmaceutics · 2026Article
- Spatial associations between neuronal membrane damage and vasculature after repetitive diffuse TBI in pigs.Acta neuropathologica communications · 2026Article
- Neuron-targeted 2-deoxyglucose-dendrimer-rosiglitazone nanotherapy mitigates neuroinflammation and cognitive deficits in pediatric traumatic brain injury.Bioengineering & translational medicine · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- From Traumatic Brain Injury to Alzheimer's Disease: Multilevel Biomechanical, Neurovascular, and Molecular Mechanisms with Emerging Therapeutic Directions.International journal of molecular sciences · 2026Review
- Subarachnoid cisterns as surgical corridors: Integrating microsurgical anatomy and neuroimaging for intracranial navigation.Surgical neurology international · 2026Review
- Exploring NanoherbalIranian journal of medical sciences · 2025Article
- Blocking axon-glial mechanotransduction to prevent concussive brain injury.Acta neuropathologica communications · 2025Article
- Mechanobiology of the blood-brain barrier during development, disease and ageing.Nature communications · 2025Review
- Actuated Hydrogel Platforms To Study Brain Cell Behavior.Advanced healthcare materials · 2025Review
- Computational Modelling of Protected and Unprotected Head Impacts in Rugby.Bioengineering (Basel, Switzerland) · 2025Article
- A cellulosic fibre foam as a bicycle helmet impact liner for brain injury mitigation in oblique impacts.Heliyon · 2025Article
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 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is distinct from other neurological disorders because it is induced by a discrete event that applies extreme mechanical forces to the brain. This review describes how the brain senses, integrates, and responds to forces under both normal conditions and during injury. The response to forces is influenced by the unique mechanical properties of brain tissue, which differ by region, cell type, and sub-cellular structure. Elements such as the extracellular matrix, plasma membrane, transmembrane receptors, and cytoskeleton influence its properties. These same components also act as force-sensors, allowing neurons and glia to respond to their physical environment and maintain homeostasis. However, when applied forces become too large, as in TBI, these components may respond in an aberrant manner or structurally fail, resulting in unique pathological sequelae. This so-called "pathological mechanosensation" represents a spectrum of cellular responses, which vary depending on the overall biomechanical parameters of the injury and may be compounded by repetitive injuries. Such aberrant physical responses and/or damage to cells along with the resulting secondary injury cascades can ultimately lead to long-term cellular dysfunction and degeneration, often resulting in persistent deficits. Indeed, pathological mechanosensation not only directly initiates secondary injury cascades, but this post-physical damage environment provides the context in which these cascades unfold. Collectively, these points underscore the need to use experimental models that accurately replicate the biomechanics of TBI in humans. Understanding cellular responses in context with injury biomechanics may uncover therapeutic targets addressing various facets of trauma-specific sequelae.
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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.