ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2020
Molecular switching from ubiquitin-proteasome to autophagy pathways in mice stroke model.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Epigenetic Mechanisms Regulating Ferroptosis in Ischemic Stroke: From Pathogenesis to Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- The deubiquitinase OTUD3 plays a neuroprotective role by reducing ferroptosis induced by cerebral ischaemia reperfusion via stabilizing PLK1 via deubiquitination.Clinical and translational medicine · 2025Article
- Targeting intracellular autophagic process for the treatment of post-stroke ischemia/reperfusion injury.Animal models and experimental medicine · 2025Review
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- A temperature-ultrasound sensitive nanoparticle delivery system for exploring central neuroinflammation mechanism in stroke-heart syndrome.Journal of nanobiotechnology · 2024Article
- Interactions Between Ferroptosis and Oxidative Stress in Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2024Review
- Identification of Autophagy-Related Biomarkers and Diagnostic Model in Alzheimer's Disease.Genes · 2024Article
- SLC15A3 plays a crucial role in pulmonary fibrosis by regulating macrophage oxidative stress.Cell death and differentiation · 2024Article
- The Multiple Roles of Autophagy in Neural Function and Diseases.Neuroscience bulletin · 2024Review
- Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes.International journal of molecular sciences · 2023Review
- Within the Ischemic Penumbra, Sub-Cellular Compartmentalization of Heat Shock Protein 70 Overlaps with Autophagy Proteins and Fails to Merge with Lysosomes.Molecules (Basel, Switzerland) · 2022Article
- Inflammation: A New Look at an Old Problem.International journal of molecular sciences · 2022Review
- Research progress on astrocyte autophagy in ischemic stroke.Frontiers in neurology · 2022Review
- The Autophagy-Related Organelle Autophagoproteasome Is Suppressed within Ischemic Penumbra.International journal of molecular sciences · 2021Article
- Tomatidine provides mitophagy-independent neuroprotection after ischemic injury.FEBS open bio · 2021Article
- Celecoxib-Dependent Neuroprotection in a Rat Model of Transient Middle Cerebral Artery Occlusion (tMCAO) Involves Modifications in Unfolded Protein Response (UPR) and Proteasome.Molecular neurobiology · 2021Article
- Elevated post-ischemic ubiquitination results from suppression of deubiquitinase activity and not proteasome inhibition.Cellular and molecular life sciences : CMLS · 2021Article
- Co-Chaperone Bag-1 Plays a Role in the Autophagy-Dependent Cell Survival through Beclin 1 Interaction.Molecules (Basel, Switzerland) · 2021Article
- Characterization of Histone Deacetylase Mechanisms in Cancer Development.Frontiers in oncology · 2021Review
- The Role of Autophagy in the Pathogenesis of Ischemic Stroke.Current neuropharmacology · 2021Review
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Authors and funding
11 authors.
Funding
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Abstract
The ubiquitin-proteasome system (UPS) and autophagy are two major pathways to degrade misfolded proteins that accumulate under pathological conditions. When UPS is overloaded, the degeneration pathway may switch to autophagy to remove excessive misfolded proteins. However, it is still unclear whether and how this switch occurs during cerebral ischemia. In the present study, transient middle cerebral artery occlusion (tMCAO) resulted in accelerated ubiquitin-positive protein aggregation from 0.5 h of reperfusion in mice brain after 10, 30 or 60 min of tMCAO. In contrast, significant reduction of p62 and induction of LC3-II were observed, peaking at 24 h of reperfusion after 30 and 60 min tMCAO. Western blot analyses showed an increase of BAG3 and HDAC6 at 1 or 24 h of reperfusion that was dependent on the ischemic period. In contract, BAG1 decreased at 24 h of reperfusion after 10, 30 or 60 min of tMCAO after double immunofluorescent colocalization of ubiquitin, HSP70, p62 and BAG3. These data suggest that a switch from UPS to autophagy occurred between 10 and 30 min of cerebral ischemia depending on the BAG1/BAG3 ratio and level of HDAC6.
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