ReviewNeurotoxicity research2021
Understanding Abnormal c-JNK/p38MAPK Signaling Overactivation Involved in the Progression of Multiple Sclerosis: Possible Therapeutic Targets and Impact on Neurodegenerative Diseases.
Review in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- GPCR-Driven Muscarinic M1 and Histamine H1 Receptor Signaling Converging on the PI3K/Akt/mTOR Pathway: Functional Integration in Neuroinflammation and Myelin Repair in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Combined Puerarin and Magnesium Acetyl Taurate Intervention Mitigates Autism-Like Pathology Through Glutamatergic and MAPK Pathway Regulation.Neurochemical research · 2026Article
- Unlocking the aging brain: mTORC1 as a convergent integrator for neurodegeneration and therapeutic intervention.Biogerontology · 2026Review
- Alisol A Mitigates Neuroinflammation and Oxidative Stress After Subarachnoid Hemorrhage Through SIRT3-Driven Reprogramming of Mitochondrial Metabolism.Molecular neurobiology · 2026Article
- Aberrant maintenance of developmental transcription factor PAX6 promotes neuronal cell death via JNK3 signaling.Cell death & disease · 2026Article
- Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Pharmacological Inhibition of JNK Signalling Exerts Anti-Neoplastic Effects on SH-SY5Y Human Neuroblastoma Cells.International journal of molecular sciences · 2025Article
- Neuroprotective Effect of Rosuvastatin Calcium Combined with Hyperbaric Oxygen Mediated p38MAPK Pathway in Rats with Leukoaraiosis.Cell biochemistry and biophysics · 2025Article
- Equol as a Multitarget Agent Against Neurodegeneration: Mechanistic Insights into Its Molecular Modulation.Neuromolecular medicine · 2025Review
- CircITSN1/EIF4A3/Itsn1 axis mediates postoperative cognitive dysfunction in aged mice: A novel mechanism and therapeutic target.Molecular therapy. Nucleic acids · 2025Article
- Article
- Construction of epilepsy diagnosis model based on cell senescence-related genes and its potential mechanism.Frontiers in neurology · 2025Article
- The Polygenic Nature of Multiple Sclerosis: Genetic Variants, Immunological Modulation, and Environmental Connections.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Neurodevelopmental disorders and gut-brain interactions: exploring the therapeutic potential of pycnogenol through microbial-metabolic-neural networks.Frontiers in cellular and infection microbiology · 2025Review
- JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties.Cell adhesion & migration · 2024Review
- Guggulsterone Selectively Modulates STAT-3, mTOR, and PPAR-Gamma Signaling in a Methylmercury-Exposed Experimental Neurotoxicity: Evidence from CSF, Blood Plasma, and Brain Samples.Molecular neurobiology · 2024Article
- Purmorphamine, a Smo-Shh/Gli Activator, Promotes Sonic Hedgehog-Mediated Neurogenesis and Restores Behavioural and Neurochemical Deficits in Experimental Model of Multiple Sclerosis.Neurochemical research · 2024Article
- 5Z-7-Oxozaenol attenuates cuprizone-induced demyelination in mice through microglia polarization regulation.Brain and behavior · 2024Article
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents.CNS & neurological disorders drug targets · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Demyelination, immune dysregulation, and neuroinflammation are the most common triggers of motor neuron disorders such as multiple sclerosis (MS). MS is a chronic demyelinating neurodegenerative disease of the central nervous system caused by abnormal immune activation, which causes myelin sheath damage. Cell signal transduction pathways are required for a variety of physiological and pathological processes in the brain. When these signaling systems become overactive, they can lead to disease progression. In various physiological conditions, abnormal mitogen-activated protein kinase (MAPK) activation is associated with several physiological dysfunctions that cause neurodegeneration. Previous research indicates that c-JNK and p38MAPK signaling play critical roles in neuronal growth and differentiation. c-JNK/p38MAPK is a member of the MAPK family, which regulates metabolic pathways, cell proliferation, differentiation, and apoptosis that control certain neurological activities. During brain injuries, c-JNK/p38MAPK also affects neuronal elastic properties, nerve growth, and cognitive processing. This review systematically linked abnormal c-JNK/p38MAPK signaling activation to multiple neuropathological pathways in MS and related neurological dysfunctions. MS progression is linked to genetic defects, oligodendrocyte destruction, glial overactivation, and immune dysregulation. We concluded that inhibiting both the c-JNK/p38MAPK signaling pathways can promote neuroprotection and neurotrophic effects against the clinical-pathological presentation of MS and influence other neurological disorders. As a result, the potential benefits of c-JNK/p38MAPK downregulation for the development of disease-modifying treatment interventions in the future could include MS prevention and related neurocomplications.
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Registered trials
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