ArticlePloS one2019
Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Old and Promising Markers Related to Autophagy in Traumatic Brain Injury.International journal of molecular sciences · 2022Pooled it
- KDM6A/MMP-3 epigenetic axis governs macrophage senescence after spinal cord injury for mediating the regenerative niche to promote neurological repair.Journal of advanced research · 2026Article
- Selective elimination of amyloid-β-induced senescent neuroblastoma cells by Moringa oleifera leaf extract.Scientific reports · 2026Article
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- Cellular senescence and senolytic therapy in traumatic brain injury.Frontiers in neuroscience · 2026Review
- Mechanisms of cell senescence and apoptosis in cyclophosphamide-induced premature ovarian failure in rats.Journal of ovarian research · 2025Article
- Senolytic Treatment Attenuates Global Ischemic Brain Injury and Enhances Cognitive Recovery by Targeting Mitochondria.Cellular and molecular neurobiology · 2025Article
- Spatio-Temporal Characterization of Cellular Senescence Hallmarks in Experimental Ischemic Stroke.International journal of molecular sciences · 2025Article
- Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke.Translational neurodegeneration · 2024Review
- Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024Review
- Review
- Age-Related Alterations in Immune Function and Inflammation: Focus on Ischemic Stroke.Aging and disease · 2024Review
- 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
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- The potential use of ascorbic acid to recover the cellular senescence of lipopolysaccharide-induced human apical papilla cells: an in vitro study.Clinical oral investigations · 2023Article
- Article
- Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury.Neurobiology of disease · 2023Review
- Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence.International journal of molecular sciences · 2023Article
- Cellular senescence in brain aging and cognitive decline.Frontiers in aging neuroscience · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage response signaling, leading to cell disorders. TBI initially activates the cell cycle followed by the subsequent triggering of senescence. This study aims to clarify how the mRNA and protein expression of different markers of cell cycle and senescence are modulated and switched over time after TBI. We performed senescence-associated-β-galactosidase (SA-β-gal) staining, immunohistochemical analysis, and real-time PCR to examine the time-dependent changes in expression levels of proteins and mRNA, related to cell cycle and cellular senescence markers, in the cerebrum during the initial 14 days after TBI using a mouse model of controlled cortical impact (CCI). Within the area adjacent to the cerebral contusion after TBI, the protein and/or mRNA expression levels of cell cycle markers were increased significantly until 4 days after injury and senescence markers were significantly increased at 4, 7, and 14 days after injury. Our findings suggested that TBI initially activated the cell cycle in neurons, astrocytes, and microglia within the area adjacent to the hemicerebrum contusion in TBI, whereas after 4 days, such cells could undergo senescence in a cell-type-dependent manner.
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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.