ReviewCell proliferation2022
The PI3K/AKT signalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities.
Review in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 2 of them syntheses that pooled it.
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Who cites it
172 citing papers in PubMed, 2 syntheses or guidelines pooled it, 285 citations in OpenAlex.
- A bibliometric analysis of the research hotspots and frontiers related to cell death in spinal cord injury.Frontiers in neurology · 2023Pooled it
- The efficacy and potential pharmacological mechanism of Fufang Danshen Tablet in promoting the rehabilitation of ischemic stroke: a meta-analysis andFrontiers in neurologyPooled it
- ROS-responsive hydrogel delivering liposomal indole-3-propionic acid promotes spinal cord injury repair by enhancing CX3CL1-CX3CR1 mediated neuron-microglia communication.Materials today. Bio · 2026Article
- Morpho-crystallo-electronic Co-optimization of PtAu/GOx nanozyme for enhanced NIR-II photothermal-cascade catalytic tumor therapy.Materials today. Bio · 2026Article
- Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.Inflammopharmacology · 2026Review
- Review
- Article
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- Magnesium and nerve injury: Mechanisms and applications.Neural regeneration research · 2026Article
- Natural Products Targeting Airway Inflammation and Mucus Hypersecretion: Molecular Mechanisms and Therapeutic Potential for Respiratory Health.Nutrients · 2026Review
- Dual Inhibition of PI3K-AKT Signaling Pathway by miR-542 Overexpression in Cervical Cancer.Biochemical genetics · 2026Article
- The Association Between Potential Nuclear Factor-Kappa B1 Gene Polymorphism rs28362491 and miR-206 Level in Patients With Acute Lymphoblastic Leukemia.World journal of oncology · 2026Article
- Interferon regulatory factor 4-releasing 3D-printed scaffolds enhance spinal cord repair by modulating macrophage polarization.Neural regeneration research · 2026Article
- LACC1 attenuates LPS-induced acute lung injury by inhibiting inflammatory response in alveolar macrophage through LPAR3/PI3K/AKT/mTOR signaling pathway.Biomarker research · 2026Article
- SVF Combined with HGF-Functionalized Self-Assembling Peptide Hydrogel Promotes Spinal Cord Injury Repair in Rats.Gels (Basel, Switzerland) · 2026Article
- Overcoming Barriers to Axonal Regeneration in Spinal Cord Injury: Mechanistic Insights and Therapeutic Frontiers.CNS neuroscience & therapeutics · 2026Review
- Thrombospondin-4 Regulates Lipopolysaccharide-Induced Apoptosis and Inflammation in Nucleus Pulposus Cells via the Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway.Immunity, inflammation and disease · 2026Article
- Recent advances on anti-scarring properties of amniotic membrane: emerging strategies and clinical potentials in regenerative medicine.Stem cell research & therapy · 2026Review
- TRIM33 Reverses Cisplatin Resistance in Non-Small Cell Lung Cancer by Regulating the PI3K/AKT Pathway via Ubiquitination-Mediated Degradation of LPCAT1.World journal of oncology · 2026Article
- Development of aBioactive materials · 2026Article
112 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
objectsTraumatic spinal cord injury (TSCI) causes neurological dysfunction below the injured segment of the spinal cord, which significantly impacts the quality of life in affected patients. The phosphoinositide 3kinase/serine-threonine kinase (PI3K/AKT) signaling pathway offers a potential therapeutic target for the inhibition of secondary TSCI. This review summarizes updates concerning the role of the PI3K/AKT pathway in TSCI. MATERIALS AND
methodsBy searching articles related to the TSCI field and the PI3K/AKT signaling pathway, we summarized the mechanisms of secondary TSCI and the PI3K/AKT signaling pathway; we also discuss current and potential future treatment methods for TSCI based on the PI3K/AKT signaling pathway.
resultsEarly apoptosis and autophagy after TSCI protect the body against injury; a prolonged inflammatory response leads to the accumulation of pro-inflammatory factors and excessive apoptosis, as well as excessive autophagy in the surrounding normal nerve cells, thus aggravating TSCI in the subacute stage of secondary injury. Initial glial scar formation in the subacute phase is a protective mechanism for TSCI, which limits the spread of damage and inflammation. However, mature scar tissue in the chronic phase hinders axon regeneration and prevents the recovery of nerve function. Activation of PI3K/AKT signaling pathway can inhibit the inflammatory response and apoptosis in the subacute phase after secondary TSCI; inhibiting this pathway in the chronic phase can reduce the formation of glial scar.
conclusionThe PI3K/AKT signaling pathway has an important role in the recovery of spinal cord function after secondary injury. Inducing the activation of PI3K/AKT signaling pathway in the subacute phase of secondary injury and inhibiting this pathway in the chronic phase may be one of the potential strategies for the treatment of TSCI.
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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.