ArticleCNS neuroscience & therapeutics2017
KLF4 Knockdown Attenuates TBI-Induced Neuronal Damage through p53 and JAK-STAT3 Signaling.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- The utilization of small non-mammals in traumatic brain injury research: A systematic review.CNS neuroscience & therapeutics · 2021Pooled it
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Integrative assessment of RNA sequencing and in silico analysis to pinpoint mRNAs, lncRNAs, and circRNAs interactions with miRNAs underlying arsenic-induced neurotoxicity.BMC genomics · 2025Article
- Eyes Are the Windows to the Soul: Reviewing the Possible Use of the Retina to Indicate Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Association of MicroRNA-146a-5p Polymorphism with Cognitive Impairment in Adolescents with Depressive Disorder.Molecular syndromology · 2025Article
- Krüppel-like factor 4 transcription factor in blood-brain barrier endothelial cells: A potential role in Alzheimer's disease.Animal models and experimental medicine · 2025Review
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Targeting STAT3 signaling pathway by curcumin and its analogues for breast cancer: A narrative review.Animal models and experimental medicine · 2024Review
- Effect of Kruppel-like factor 4 on PTZ-induced acute seizure mice.Journal of cellular and molecular medicine · 2024Article
- Therapeutic Targeting of Krüppel-Like Factor 4 and Its Pharmacological Potential in Parkinson's Disease: a Comprehensive Review.Molecular neurobiology · 2024Review
- Endoplasmic reticulum stress and the unfolded protein response: emerging regulators in progression of traumatic brain injury.Cell death & disease · 2024Review
- Identification and validation of autophagy-related genes in primary open-angle glaucoma.BMC medical genomics · 2023Article
- Reduced cerebral cortex thickness is related to overexpression of exosomal miR-146a-5p in medication-free patients with major depressive disorder.Psychological medicine · 2023Article
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
- Transcription factors are potential therapeutic targets in epilepsy.Journal of cellular and molecular medicine · 2022Review
- Microglia secrete miR-146a-5p-containing exosomes to regulate neurogenesis in depression.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Neuro-Visual and Vestibular Manifestations of Concussion and Mild TBI.Current neurology and neuroscience reports · 2022Review
- Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury.Neural regeneration research · 2022Article
- Aerobic Exercise Improves Type 2 Diabetes Mellitus-Related Cognitive Impairment by Inhibiting JAK2/STAT3 and Enhancing AMPK/SIRT1 Pathways in Mice.Disease markers · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTraumatic brain injury (TBI) is induced by complex primary and secondary mechanisms that give rise to cell death, inflammation, and neurological dysfunction. Understanding the mechanisms that drive neurological damage as well as those that promote repair can guide the development of therapeutic drugs for TBI. Kruppel-like factor 4 (KLF4) has been reported to negatively regulate axon regeneration of injured retinal ganglion cells (RGCs) through inhibition of JAK-STAT3 signaling. However, the role of KLF4 in TBI remains unreported. Reactive oxygen species (ROS)-induced neuronal death is a pathophysiological hallmark of TBI.
methodsIn this study, we used H
resultsThe results show that H
conclusionThese findings provide evidence that KLF4 plays an important role in the pathophysiology of TBI. Blocking KLF4 may be a potential therapeutic strategy for the treatment of TBI, either alone or in combination with agents that target complementary mechanisms.
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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.