ArticleAmerican journal of translational research2020
MEK inhibitor trametinib attenuates neuroinflammation and cognitive deficits following traumatic brain injury in mice.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 20 citations in OpenAlex.
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- Trauma-associated extracellular histones mediate inflammation via a MYD88-IRAK1-ERK signaling axis and induce lytic cell death in human adipocytes.Cell death & disease · 2024Article
- Trametinib ameliorates aging-associated gut pathology inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Nicorandil attenuates cognitive impairment after traumatic brain injury via inhibiting oxidative stress and inflammation: Involvement of BDNF and NGF.Brain and behavior · 2024Article
- Astrocyte-derived exosomal lncRNA 4933431K23Rik modulates microglial phenotype and improves post-traumatic recovery via SMAD7 regulation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Trametinib-Induced Epidermal Thinning Accelerates a Mouse Model of Junctional Epidermolysis Bullosa.Biomolecules · 2023Article
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- BAY61‑3606 attenuates neuroinflammation and neurofunctional damage by inhibiting microglial Mincle/Syk signaling response after traumatic brain injury.International journal of molecular medicine · 2022Article
- MEK1/2 Inhibitor (GDC0623) Promotes Osteogenic Differentiation of Primary Osteoblasts Inhibited by IL-1International journal of endocrinology · 2021Article
- Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia-mediated neuroinflammation is one of the hallmark pathological features following traumatic brain injury (TBI) that contributes to aggravated brain damage and cognitive deficits. These pathologies require novel effective treatments to improve prognosis. Trametinib, a mitogen-activated protein kinase inhibitor approved by the Food and Drug Administration in treating various malignant tumors, has been shown to exert anti-inflammatory effects. The present study demonstrated that TBI mice treated with trametinib exhibited improved cognitive function. Trametinib treatment rescued oligodendrocytes and decreased infiltrating microglial density in the TBI area. Furthermore, this study revealed that ameliorated lipopolysaccharides (LPS) induced inflammatory reaction in microglial cells. Besides, trametinib attenuated inflammation factors expression during the early stages of TBI. In addition, trametinib inhibited LPS-induced microglial chemotactic activity. In conclusion, the results indicate that trametinib efficiently suppresses microglia-induced neuroinflammation and improves cognitive function of TBI mice, providing a potential therapy strategy for TBI patients.
Indexed as
Identifiers
33194035PMC7653601W3100895015What 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.