ArticleNeurobiology of disease2018
Activation of cyclin D1 affects mitochondrial mass following traumatic brain injury.
Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Enduring Effects of Humanin on Mitochondrial Systems in TBI Pathology.Biomolecules · 2025Article
- Pterostilbene improves neurological dysfunction and neuroinflammation after ischaemic stroke via HDAC3/Nrf1-mediated microglial activation.Cellular & molecular biology letters · 2024Article
- Intranasal delivery of mitochondria targeted neuroprotective compounds for traumatic brain injury: screening based on pharmacological and physiological properties.Journal of translational medicine · 2024Review
- Aberrant ER Stress Induced Neuronal-IFNβ Elicits White Matter Injury Due to Microglial Activation and T-Cell Infiltration after TBI.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Histone Deacetylase 4 Downregulation Elicits Post-Traumatic Psychiatric Disorders through Impairment of Neurogenesis.Journal of neurotrauma · 2019Article
- Aberrant cell cycle induction is pivotal for mitochondrial biogenesis after traumatic brain injury.Neural regeneration research · 2019Article
- An augmentation in histone dimethylation at lysine nine residues elicits vision impairment following traumatic brain injury.Free radical biology & medicine · 2019Article
- Understanding the link between traumatic brain injury and Alzheimer's disease.Annals of translational medicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cell cycle activation has been associated with varying types of neurological disorders including brain injury. Cyclin D1 is a critical modulator of cell cycle activation and upregulation of Cyclin D1 in neurons contributes to the pathology associated with traumatic brain injury (TBI). Mitochondrial mass is a critical factor to maintain the mitochondrial function, and it can be regulated by different signaling cascades and transcription factors including NRF1. However, the underlying mechanism of how TBI leads to impairment of mitochondrial mass following TBI remains obscure. Our results indicate that augmentation of CyclinD1 attenuates mitochondrial mass formation following TBI. To elucidate the molecular mechanism, we found that Cyclin D1 interacts with a transcription factor NRF1 in the nucleus and prevents NRF1's interaction with p300 in the pericontusional cortex following TBI. As a result, the acetylation level of NRF1 was decreased, and its transcriptional activity was attenuated. This event leads to a loss of mitochondrial mass in the pericontusional cortex following TBI. Intranasal delivery of Cyclin D1 RNAi immediately after TBI rescues transcriptional activation of NRF1 and recovers mitochondrial mass after TBI.
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Registered trials
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