ArticleExperimental neurology2021
Interruption of endolysosomal trafficking leads to stroke brain injury.
Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Interruption of Endolysosomal Trafficking After Focal Brain Ischemia.Frontiers in molecular neuroscience · 2021Pooled it
- Animal models for investigating post-stroke cognitive impairment: A neurovascular trafficking perspective.Animal models and experimental medicine · 2026Review
- Inhibition of Cathepsin B Ameliorates Murine Cognitive Dysfunction and Neuronal Damage in Ischemic Stroke by Inhibiting Mitochondrial Apoptosis and Drp1-Mediated Mitochondrial Fission.Molecular neurobiology · 2025Article
- Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection.Cell death & disease · 2025Article
- Dual role for pannexin 1 at synapses: regulating functional and morphological plasticity.The Journal of physiology · 2025Review
- The role of autophagy in ischemic brain injury.Autophagy reports · 2025Review
- N-ethylmaleimide-sensitive factor elicits a neuroprotection against ischemic neuronal injury by restoring autophagic/lysosomal dysfunction.Cell death discovery · 2024Article
- Unveiling the mechanisms and challenges of cancer drug resistance.Cell communication and signaling : CCS · 2024Review
- Downregulation ofFrontiers in aging neuroscience · 2024Article
- The role of synaptic protein NSF in the development and progression of neurological diseases.Frontiers in neuroscience · 2024Review
- The Pathological Mechanism of Neuronal Autophagy-Lysosome Dysfunction After Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- The critical role of the endolysosomal system in cerebral ischemia.Neural regeneration research · 2023Review
- Monocyte, neutrophil, and whole blood transcriptome dynamics following ischemic stroke.BMC medicine · 2023Article
- CTSB is a negative prognostic biomarker and therapeutic target associated with immune cells infiltration and immunosuppression in gliomas.Scientific reports · 2022Article
- An update on the unfolded protein response in brain ischemia: Experimental evidence and therapeutic opportunities.Neurochemistry international · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
background and purposeDysfunction of the endolysosomal system can cause cell death. A key molecule for controlling the endolysosomal trafficking activities is the N-ethylmaleimide-sensitive factor (NSF) ATPase. This study investigates the cascades of NSF ATPase inactivation events, endolysosomal damage, cathepsin release, and neuronal death after focal brain ischemia.
methodsA total of 62 rats were used in this study. They were subjected to sham surgery or 2 h of focal brain ischemia followed by 1, 4, and 24 h of reperfusion. Confocal microscopy and Western blot analysis were utilized to analyze the levels, redistribution, and co-localization of key proteins of the Golgi apparatus, late endosomes, endolysosomes, and lysosomes. Light and electron microscopy were used to examine the histopathology, protein aggregation, and endolysosomal ultrastructures.
resultsTwo hours of focal brain ischemia in rats led to acute neuronal death at the striatal core in 4 h and a slower type of neuronal death in the neocortical area during 1-24 h reperfusion periods. Confocal microscopy showed that NSF immunoreactivity was irreversibly and selectively depleted from most, if not all, post-ischemic penumbral neurons. Western blot analysis further demonstrated that NSF depletion from brain sections was due to its deposition into dense inactive aggregates that could not be recognized by the NSF antibody. Commitantly, the Golgi apparatus was completely fragmented and cathepsin B (CTSB)-containing endolysosomal structures, as well as p62/SQSTM1- and EEA1-immunopositive structures were massively accumulated in the post-ischemic penumbral neurons. Ultimately, CTSB was released into the cytoplasm and extracellular space, causing stroke brain injury.
conclusionStroke Inactivates NSF, resulting in disruption of the reforming of functional endolysosomal compartments, blockade of the endocytic and autophagic pathways, a large scale of CTSB release into the cytoplasm and extracellular space, and stroke brain injury in the rat model.
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