ReviewInternational journal of molecular sciences2018
Stress-Activated Protein Kinases in Spinal Cord Injury: Focus on Roles of p38.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.Inflammopharmacology · 2026Review
- High-linear energy transfer radiation disrupts natural killer cell surveillance of senescent intestinal cells in the mouse intestine.Molecular biomedicine · 2026Article
- Obacunone Promotes Functional Recovery After Spinal Cord Injury by Attenuating Neuroinflammation by Targeting the TLR4/MyD88/p38 MAPK Pathway.Drug design, development and therapy · 2026Article
- High-Quality In Vivo Chemical Probes for Protein Kinases Disclosed in 2024.ACS pharmacology & translational science · 2025Review
- Hamayou () protein hydrolysate ameliorates depression by regulating the mitogen-activated protein kinase pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Genome-wide screening of mitogen-activated protein kinase (MAPK) gene family and expression profile under heavy metal stress in Solanum lycopersicum.Biotechnology letters · 2025Article
- Identification and experimental validation of BMX as a crucial PANoptosis‑related gene for immune response in Spinal Cord Injury.PloS one · 2025Article
- Advances of the MAPK pathway in the treatment of spinal cord injury.CNS neuroscience & therapeutics · 2024Review
- Translational Relevance of Secondary Intracellular Signaling Cascades Following Traumatic Spinal Cord Injury.International journal of molecular sciences · 2024Review
- Sex Dependent Disparities in the Central Innate Immune Response after Moderate Spinal Cord Contusion in Rat.Cells · 2024Article
- Article
- Downregulation of Circular RNA Gla Reduced Astrocyte Inflammatory Status by Regulating miR-488/MEKK1 Levels and Promoted Functional Recovery After Spinal Cord Injury.Journal of inflammation research · 2024Article
- bFGF-like Activity Supported Tissue Regeneration, Modulated Neuroinflammation, and Rebalanced CaInternational journal of molecular sciences · 2023Article
- Gelatin methacryloyl hydrogel scaffold loaded with activated Schwann cells attenuates apoptosis and promotes functional recovery following spinal cord injury.Experimental and therapeutic medicine · 2023Article
- Inhibition of Microglial GSK3β Activity Is Common to Different Kinds of Antidepressants: A Proposal for an In Vitro Screen to Detect Novel Antidepressant Principles.Biomedicines · 2023Review
- Molecular Aspects of Hypoxic Stress Effects in Chronic Ethanol Exposure of Neuronal Cells.Current issues in molecular biology · 2023Article
- Isoimperatorin therapeutic effect against aluminum induced neurotoxicity in albino mice.Frontiers in pharmacology · 2023Article
- Mesenchymal stem cells in the treatment of spinal cord injury: Mechanisms, current advances and future challenges.Frontiers in immunology · 2023Review
- Apoptosis and (in) Pain-Potential Clinical Implications.Biomedicines · 2022Review
- Article
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
Spinal cord injury (SCI) consists of three phases-acute, secondary, and chronic damages-and limiting the development of secondary damage possibly improves functional recovery after SCI. A major component of the secondary phase of SCI is regarded as inflammation-triggered events: induction of cytokines, edema, microglial activation, apoptosis of cells including oligodendrocytes and neurons, demyelination, formation of the astrocytic scar, and so on. Two major stress-activated protein kinases (SAPKs)-c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK)-are activated in various types of cells in response to cellular stresses such as apoptotic stimuli and inflammatory waves. In animal models of SCI, inhibition of either JNK or p38 has been shown to promote neuroprotection-associated functional recovery. Here, we provide an overview on the roles of SAPKs in SCI and, in particular, the pathological role of p38 will be discussed as a promising target for therapeutic intervention in SCI.
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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 Socratic graph.