ArticleJournal of neuroinflammation2020
Disruption of Midkine gene reduces traumatic brain injury through the modulation of neuroinflammation.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- Midkine (MDK) as a central regulator of the tumor microenvironment: From developmental cytokine to therapeutic target.Cancer letters · 2026Review
- Midkine Overexpression Promotes Functional Recovery After Spinal Cord Injury by Enhancing Microglial Efferocytosis Via LRP-1.CNS neuroscience & therapeutics · 2026Article
- Pleiotrophin/Midkine Pathway Is Dysregulated in a TDP-43Neuropathology : official journal of the Japanese Society of Neuropathology · 2026Article
- Midkine-Mediated Microglia Activation after Renal Injury Promotes Cognitive Impairment Following Ischemic Renal Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Stress-Induced Activation of Prolactin-NR4A1-Midkine Axis Exacerbates Skin Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microbial production of short-chain fatty acids attenuates long-term neurologic impairment after traumatic brain injury.Journal of neuroinflammation · 2025Article
- Glutamate Exacerbates Traumatic Brain Injury-Induced Acute Lung Injury Through NMDAR/ROS/CaThe Kaohsiung journal of medical sciences · 2025Article
- Single-cell analysis reveals shared and distinct molecular signatures in brain organoid models of neurodegeneration and neuroinflammation.Alzheimer's research & therapy · 2025Article
- DTX1 Modulates Microglial M1 Polarization and Exacerbates Neuroinflammation in Traumatic Brain Injury Model Rats through NF-κB/IRF5.Molecular neurobiology · 2025Article
- Midkine (MDK) in cancer and drug resistance: from inflammation to therapy.Discover oncology · 2025Review
- Cocaine perturbs neurodevelopment and increases neuroinflammation in a prenatal cerebral organoid model.Translational psychiatry · 2025Article
- Single cell deciphering of pruritic keloids: the interaction between fibroblasts and Schwann cells through the Midkine signaling.Burns & trauma · 2025Article
- Identification of mRNA biomarkers in extremely early hypertensive intracerebral hemorrhage (HICH).Proteome science · 2024Article
- Data-independent acquisition proteomic analysis of the brain microvasculature in Alzheimer's disease identifies major pathways of dysfunction and upregulation of cytoprotective responses.Fluids and barriers of the CNS · 2024Article
- Midkine: A Cancer Biomarker Candidate and Innovative Therapeutic Approaches.European journal of breast health · 2024Article
- Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome.Neurochemical research · 2024Article
- Editorial: Trends in neuroimmunology: cross-talk between brain-resident and peripheral immune cells in both health and disease.Frontiers in immunology · 2024Article
- Extracellular cold-inducible RNA-binding protein mediated neuroinflammation and neuronal apoptosis after traumatic brain injury.Burns & trauma · 2024Article
- Single-cell RNA-sequencing analysis reveals enhanced non-canonical neurotrophic factor signaling in the subacute phase of traumatic brain injury.CNS neuroscience & therapeutics · 2023Article
- Prospects for Nerve Regeneration and Gene Therapy in the Treatment of Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMidkine (MK) is a multifunctional cytokine found upregulated in the brain in the presence of different disorders characterized by neuroinflammation, including neurodegenerative disorders and ischemia. The neuroinflammatory response to traumatic brain injury (TBI) represents a key secondary injury factor that can result in further neuronal injury. In the present study, we investigated the role of endogenous MK in secondary injury, including neuroinflammation, immune response, and neuronal apoptosis activity, after TBI.
methodsWild type (Mdk
resultsAs opposed to Mdk
conclusionOur findings suggest that MK-deficiency reduced tissue infiltration of microglia/macrophages and altered their polarization status thereby reducing neuroinflammation, neuronal apoptosis, and tissue loss and improving neurological outcomes after TBI. Therefore, targeting MK to modulate neuroinflammation may represent a potential therapeutic strategy for TBI management.
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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.