ArticleMediators of inflammation2022
Enriched Environment-Induced Neuroprotection against Cerebral Ischemia-Reperfusion Injury Might Be Mediated via Enhancing Autophagy Flux and Mitophagy Flux.
Article in Mediators of inflammation, 2022. 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.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Is environmental enrichment effective in modulating autophagy markers in the brain exposed to adverse conditions? A systematic review.Frontiers in cellular neuroscience · 2025Pooled it
- Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review).Molecular medicine reports · 2026Review
- Enriched Environment Enhances Motor Function in Mice With Cerebral Infarction by Promoting mTOR-Dependent Autophagy in the Contralateral Dentate Nucleus.The Kaohsiung journal of medical sciences · 2026Article
- The role of STAT3 in regulating ferroptosis in cancer: molecular mechanisms and targeted therapeutic perspectives.Cancer gene therapy · 2026Review
- Molecular Pathophysiology of Ischemic Stroke and Mesenchymal Stem Cell Based Therapeutic Strategies for Neural Tissue Regeneration: A Pre-clinical and Clinical Perspective.Stem cell reviews and reports · 2026Review
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Enriched Environment Ameliorates Cerebral Ischemia-Reperfusion Injury via Dopamine-HAntioxidants (Basel, Switzerland) · 2025Article
- A Scoping Review of Preclinical Environmental Enrichment Protocols in Models of Poststroke to Set the Foundations for Translating the Paradigm to Clinical Settings.Translational stroke research · 2025Article
- Targeting Drp1 in Cerebral Ischemia-Reperfusion Injury: Mechanisms and Therapeutic Implications.CNS neuroscience & therapeutics · 2025Review
- Environmental enrichment: a neurostimulatory approach to aging and ischemic stroke recovery and rehabilitation.Biogerontology · 2025Review
- Relationship between enriched environment and neurodegeneration: a review from mechanism to therapy.Clinical epigenetics · 2025Review
- Esculetin attenuates cerebral ischemia-reperfusion injury and protects neurons through Nrf2 activation in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Calycosin Ameliorates Neuroinflammation via TLR4-Mediated Signal Following Cerebral Ischemia/Reperfusion Injury in vivo and in vitro.Journal of inflammation research · 2024Article
- Targeting neuronal mitophagy in ischemic stroke: an update.Burns & trauma · 2023Review
- Demand Coupling Drives Neurodegeneration: A Model of Age-Related Cognitive Decline and Dementia.Cells · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Enriched environment (EE) can protect the brain against damages caused by an ischemic stroke; however, the underlying mechanism remains elusive. Autophagy and mitochondria quality control are instrumental in the pathogenesis of ischemic stroke. In this study, we investigated whether and how autophagy and mitochondria quality control contribute to the protective effect of EE in the acute phase of cerebral ischemia-reperfusion injury. Methods: We exposed transient middle cerebral artery occlusion (tMCAO) mice to EE or standard condition (SC) for 7 days and then studied them for neurological deficits, autophagy and inflammation-related proteins, and mitochondrial morphology and function. Results: Compared to tMCAO mice in the SC group, those in the EE group showed fewer neurological deficits, relatively downregulated inflammation, higher LC3 expression, higher mitochondrial Parkin levels, higher mitochondrial fission factor dynamin-related protein-1 (Drp1) levels, lower p62 expression, and lower autophagy inhibitor mTOR expression. Furthermore, we found that the EE group showed a higher number of mitophagosomes and normal mitochondria, fewer mitolysosomes, and relatively increased mitochondrial membrane potential. Conclusion: These results suggested that EE enhances autophagy flux by inhibiting mTOR and enhances mitophagy flux via recruiting Drp1 and Parkin to eliminate dysfunctional mitochondria, which in turn inhibits inflammation and alleviates neurological deficits.
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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.