ArticleCell death & disease2019
AKT-dependent and -independent pathways mediate PTEN deletion-induced CNS axon regeneration.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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The trial behind it
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Who cites it
43 citing papers in PubMed, 64 citations in OpenAlex.
- Translational dysregulation as a mechanistic driver of cognitive, behavioral, and affective phenotypes in FXS and TSC.Neuroscience and biobehavioral reviews · 2026Review
- Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration in adult zebrafish.iScience · 2026Article
- Enhancing peripheral nerve regeneration in aging: the role of Schwann cells, c-Jun, and emerging therapeutic strategies.GeroScience · 2026Review
- Deficiency of PTEN Confers Hypersensitivity to Fatty Acid-Mediated ER Stress in Transformed Hepatocytes.International journal of molecular sciences · 2026Article
- Bone mesenchymal stem cells attenuate axonopathy in spinal cord of rats exposed to 2,5-hexanedione via NGF-dependent and -independent pathways.Molecular and cellular biochemistry · 2026Article
- Actin depolymerization promotes axon regeneration by restoring axonal mitochondrial transport in mouse models of optic neuropathy.Science translational medicine · 2026Article
- From Regeneration Failure to Functional Restoration: Unlocking the Neuronal-Intrinsic Regenerative Capacity as a Therapeutic Frontier for Optic Neuropathy and Glaucoma.CNS neuroscience & therapeutics · 2026Review
- Rat adipose-derived mesenchymal stem cell-derived exosomes loaded with miR-375 promote neurite outgrowth and peripheral nerve regeneration via activation of Akt by targeting EPHA4.Regenerative therapy · 2025Article
- Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long-Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multichannel 3D-Printed Bioactive Scaffold Combined with Small Interfering RNA Delivery to Promote Neurological Recovery after Spinal Cord Injury.Research (Washington, D.C.) · 2025Article
- Article
- Nfe2l3 promotes neuroprotection and long-distance axon regeneration after injury in vivo.Experimental neurology · 2024Article
- Glycogen synthase kinase 3 signaling in neural regeneration in vivo.Journal of molecular cell biology · 2024Review
- Anti-Gene IGF-I Vaccines in Cancer Gene Therapy: A Review of a Case of Glioblastoma.Current medicinal chemistry · 2024Review
- Phosphorylated S6K1 and 4E-BP1 play different roles in constitutively active Rheb-mediated retinal ganglion cell survival and axon regeneration after optic nerve injury.Neural regeneration research · 2023Article
- RGC-specific ATF4 and/or CHOP deletion rescues glaucomatous neurodegeneration and visual function.Molecular therapy. Nucleic acids · 2023Article
- Maf1 is an intrinsic suppressor against spontaneous neural repair and functional recovery after ischemic stroke.Journal of advanced research · 2023Article
- Differential effects of SARM1 inhibition in traumatic glaucoma and EAE optic neuropathies.Molecular therapy. Nucleic acids · 2023Article
- Moving CNS axon growth and regeneration research into human model systems.Frontiers in neuroscience · 2023Review
- Longitudinal in vivo CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Phosphatase and tensin homolog (PTEN) acts as a brake for the phosphatidylinositol 3-kinase-AKT-mTOR complex 1 (mTORC1) pathway, the deletion of which promotes potent central nervous system (CNS) axon regeneration. Previously, we demonstrated that AKT activation is sufficient to promote CNS axon regeneration to a lesser extent than PTEN deletion. It is still questionable whether AKT is entirely responsible for the regenerative effect of PTEN deletion on CNS axons. Here, we show that blocking AKT or its downstream effectors, mTORC1 and GSK3β, significantly reduces PTEN deletion-induced mouse optic nerve regeneration, indicating the necessary role of AKT-dependent signaling. However, AKT is only marginally activated in PTEN-null mice due to mTORC1-mediated feedback inhibition. That combining PTEN deletion with AKT overexpression or GSK3β deletion achieves significantly more potent axonal regeneration suggests an AKT-independent pathway for axon regeneration. Elucidating the AKT-independent pathway is required to develop effective strategies for CNS axon regeneration.
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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.