ArticleNeuromolecular medicine2022
Bim Deletion Reduces Functional Deficits Following Ischemic Stroke in Association with Modulation of Apoptosis and Inflammation.
Article in Neuromolecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanisms and Therapeutic Targets of Ischemia-Reperfusion Injury in Stroke: A Narrative Review Focusing on Blood-Brain Barrier Dysfunction.Brain sciences · 2026Review
- Plasma Levels of Neuron/Glia-Derived Apoptotic Bodies, an In Vivo Biomarker of Apoptosis, Predicts Infarct Growth and Functional Outcome in Patients with Ischemic Stroke.Translational stroke research · 2025Article
- From disruption to remodeling: the evolution and therapeutic prospects of Neuroimmune Regulatory Circuitry after ischemic stroke.Frontiers in immunology · 2025Review
- The immunomodulatory mechanism of acupuncture treatment for ischemic stroke: research progress, prospects, and future direction.Frontiers in immunology · 2024Review
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- The Anti-Cancer Effect of Cinnamon Aqueous Extract: A Focus on Hematological Malignancies.Life (Basel, Switzerland) · 2023Review
- Acupuncture at GV20 and ST36 Improves the Recovery of Behavioral Activity in Rats Subjected to Cerebral Ischemia/Reperfusion Injury.Frontiers in behavioral neuroscience · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular apoptosis is a key pathological mechanism contributing to neuronal death following ischemic stroke. The pro-apoptotic Bcl-2 family protein, Bim, is an important regulator of apoptosis. In this study we investigated the effect of Bim expression on post-stroke functional outcomes, brain injury and inflammatory mechanisms. Wild type (WT) and Bim-deficient mice underwent 1-h middle cerebral artery occlusion (MCAO) followed by 23 h of reperfusion. At 24-h post-stroke, we assessed functional deficit, infarct volume, immune cell death, as well as the number of infiltrating immune cells in the brain and circulating immune cells. Bim deficiency did not affect infarct volume (P > 0.05), but resulted in less motor impairment (~ threefold greater latency to fall in hanging grip strength test, P < 0.05) and a lower median clinical score than WT mice (P < 0.05). Additionally following MCAO, Bim-deficient mice exhibited fewer myeloid cells (particularly neutrophils) in the ischemic brain hemisphere and less apoptosis of CD3
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Registered trials
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