ReviewFrontiers in aging neuroscience2021
Cellular Senescence in Traumatic Brain Injury: Evidence and Perspectives.
Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Accelerated brain aging in Veterans with posttraumatic stress symptoms and mild traumatic brain injury.Neuroimage. Reports · 2026Article
- PTSD and complex PTSD differ significantly in plasma levels of IL2 and MMP9: patterns associated with traumatic brain injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Transcription-independent induction of rapid-onset senescence is integral to healing.Nature cell biology · 2026Article
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- Aging modulation of the immune system and immunotherapy efficacy in cancer.Frontiers in immunology · 2026Review
- Navigating anterior pituitary dysfunction after traumatic brain injury: mechanisms, diagnosis, and management.Acta neurologica Belgica · 2025Review
- Aging: the wound that never starts healing.Nature communications · 2025Review
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Δ133p53α-mediated inhibition of astrocyte senescence and neurotoxicity as a possible therapeutic approach for neurodegenerative diseases.Neuroscience · 2025Review
- Bursts of brain erosion: seizures and age-dependent neurological vulnerability.Trends in molecular medicine · 2025Review
- From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.Nature reviews. Neurology · 2024Review
- Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024Review
- Bi-directional neuro-immune dysfunction after chronic experimental brain injury.Journal of neuroinflammation · 2024Article
- Article
- Senescence and SASP Are Potential Therapeutic Targets for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Art therapy and brain injury: making the invisible visible.Frontiers in psychology · 2024Article
- NLRP3-Dependent Crosstalk between Pyroptotic Macrophage and Senescent Cell Orchestrates Trauma-Induced Heterotopic Ossification During Aberrant Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Neural cell state shifts and fate loss in ageing and age-related diseases.Nature reviews. Neurology · 2023Review
- Delayed effects of radiation in adipose tissue reflect progenitor damage and not cellular senescence.GeroScience · 2023Article
- Ability of Local Clearance of Senescent Cells in Ipsilateral Hemisphere to Mitigate Acute Ischemic Brain Injury in Mice.International journal of biological sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mild traumatic brain injury (mTBI) can lead to long-term neurological dysfunction and increase one's risk of neurodegenerative disease. Several repercussions of mTBI have been identified and well-studied, including neuroinflammation, gliosis, microgliosis, excitotoxicity, and proteinopathy - however the pathophysiological mechanisms activating these pathways after mTBI remains controversial and unclear. Emerging research suggests DNA damage-induced cellular senescence as a possible driver of mTBI-related sequalae. Cellular senescence is a state of chronic cell-cycle arrest and inflammation associated with physiological aging, mood disorders, dementia, and various neurodegenerative pathologies. This narrative review evaluates the existing studies which identify DNA damage or cellular senescence after TBI (including mild, moderate, and severe TBI) in both experimental animal models and human studies, and outlines how cellular senescence may functionally explain both the molecular and clinical manifestations of TBI. Studies on this subject clearly show accumulation of various forms of DNA damage (including oxidative damage, single-strand breaks, and double-strand breaks) and senescent cells after TBI, and indicate that cellular senescence may be an early event after TBI. Further studies are required to understand the role of sex, cell-type specific mechanisms, and temporal patterns, as senescence may be a pathway of interest to target for therapeutic purposes including prognosis and treatment.
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.