ArticleNeurochemical research2015
Endogenous TGFβ1 Plays a Crucial Role in Functional Recovery After Traumatic Brain Injury Associated with Smad3 Signal in Rats.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 2 of them syntheses that pooled it.
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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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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.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.
- Traumatic MicroRNAs: Deconvolving the Signal After Severe Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Pooled it
- Cytokine Responses in Severe Traumatic Brain Injury: Where There Is Smoke, Is There Fire?Neurocritical care · 2019Pooled it
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Article
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- 'Comprehensive review of emerging drug targets in traumatic brain injury (TBI): challenges and future scope.Inflammopharmacology · 2024Review
- The contribution of the meningeal immune interface to neuroinflammation in traumatic brain injury.Journal of neuroinflammation · 2024Review
- Transforming growth factor-β1 protects mechanically injured cortical murine neurons by reducing trauma-induced autophagy and apoptosis.Frontiers in cellular neuroscience · 2024Article
- TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications.Biomedicines · 2022Review
- Anti-inflammatory Effects of Traditional Chinese Medicines on PreclinicalFrontiers in pharmacology · 2019Review
- Focal traumatic brain injury induces neuroplastic molecular responses in lumbar spinal cord.Restorative neurology and neuroscience · 2019Article
- TGF-β1 Regulation of P-JNK and L-Type Calcium Channel Cav1.2 in Cortical Neurons.Journal of molecular neuroscience : MN · 2018Article
- Improvement of Mesenchymal Stem Cell Immunomodulatory Properties by Heat-KilledFrontiers in molecular neuroscience · 2018Article
- Review
- SMAD transcription factors are altered in cell models of HD and regulate HTT expression.Cellular signalling · 2017Article
- Breviscapine reduces neuronal injury caused by traumatic brain injury insult: partly associated with suppression of interleukin-6 expression.Neural regeneration research · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β 1 (TGFβ1) has a diverse role in astrogliosis and neuronal survival, but the underlying mechanism remains to be elucidated, especially in traumatic brain injury (TBI). Here, we show that the expression of TGFβ1 was increased in the pericontusional region, accompanied with astrogliosis and neuronal loss in TBI rats. Moreover, TGFβ1 knockdown not only reduced the number of neurons and inhibited astrogliosis but also resulted in a significant neurological dysfunction in rats with TBI. Subsequently, Smad3, a key downstream signal of TGFβ1, was involved in pericontusional region after TBI. These findings therefore indicate that TGFβ1 is involved in neuroprotection and astrogliosis, via activation of down stream Smad3 signal in the brain after injury.
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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.