ArticleOxidative medicine and cellular longevity
Wnt1 neuroprotection translates into improved neurological function during oxidant stress and cerebral ischemia through AKT1 and mitochondrial apoptotic pathways.
Article in Oxidative medicine and cellular longevity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Method parameters' impact on mortality and variability in rat stroke experiments: a meta-analysis.BMC neuroscience · 2013Pooled it
- Calcitriol provides neuroprotection against cerebral ischemia-reperfusion injury through activation of the SIRT1 pathway.Anatomy & cell biology · 2026Article
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Review
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- RNA methylation and cellular response to oxidative stress-promoting anticancer agents.Cell cycle (Georgetown, Tex.) · 2023Review
- Antagonistic Interactions in Mitochondria ROS Signaling Responses to Manganese.Antioxidants (Basel, Switzerland) · 2023Article
- Antioxidants positively regulate obesity dependent circRNAs - sperm quality - functional axis.Frontiers in endocrinology · 2023Article
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- The Contribution of Wnt Signaling to Vascular Complications in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2022Review
- Cistanoside A promotes osteogenesis of primary osteoblasts by alleviating apoptosis and activating autophagy through involvement of the Wnt/β-catenin signal pathway.Annals of translational medicine · 2022Article
- Activation of Wnt/Beta-Catenin Signaling Pathway as a Promising Therapeutic Candidate for Cerebral Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2022Review
- The Role of Astrocytes in the Neurorepair Process.Frontiers in cell and developmental biology · 2021Article
- Frizzled 1 and Wnt1 as new potential therapeutic targets in the traumatically injured spinal cord.Cellular and molecular life sciences : CMLS · 2020Article
- Lipid Emulsion Improves Functional Recovery in an Animal Model of Stroke.International journal of molecular sciences · 2020Article
- Nrf2/Wnt resilience orchestrates rejuvenation of glia-neuron dialogue in Parkinson's disease.Redox biology · 2020Review
- Neuroprotection from Excitotoxic Injury by Local Administration of Lipid Emulsion into the Brain of Rats.International journal of molecular sciences · 2020Article
- Parkinson's disease, aging and adult neurogenesis: Wnt/β-catenin signalling as the key to unlock the mystery of endogenous brain repair.Aging cell · 2020Review
- Wnt Pathway: An Emerging Player in Vascular and Traumatic Mediated Brain Injuries.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Although essential for the development of the nervous system, Wnt1 also has been associated with neurodegenerative disease and cognitive loss during periods of oxidative stress. Here we show that endogenous expression of Wnt1 is suppressed during oxidative stress in both in vitro and in vivo experimental models. Loss of endogenous Wnt1 signaling directly correlates with neuronal demise and increased functional deficit, illustrating that endogenous neuronal Wnt1 offers a vital level of intrinsic cellular protection against oxidative stress. Furthermore, transient overexpression of Wnt1 or application of exogenous Wnt1 recombinant protein is necessary to preserve neurological function and rescue neurons from apoptotic membrane phosphatidylserine externalization and genomic DNA degradation, since blockade of Wnt1 signaling with a Wnt1 antibody or dickkopf related protein 1 abrogates neuronal protection by Wnt1. Wnt1 ultimately relies upon the activation of Akt1, the modulation of mitochondrial membrane permeability, and the release of cytochrome c to control the apoptotic cascade, since inhibition of Wnt1 signaling, the phosphatidylinositol 3-kinase pathway, or Akt1 activity abrogates the ability of Wnt1 to block these apoptotic components. Our work identifies Wnt1 and its downstream signaling as cellular targets with high clinical potential for novel treatment strategies for multiple disorders precipitated by oxidative stress.
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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.