ArticleMolecular neurobiology2024
Nuclear Factor Erythroid 2-Related Factor 2 is Essential for Low-Normobaric Oxygen Treatment-Mediated Blood-Brain Barrier Protection Following Ischemic Stroke.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Autophagy in ischemic stroke: from cellular survival mechanism to pathological damage.Metabolic brain disease · 2026Review
- Potential Mechanisms of Exercise-Mediated Ferroptosis Regulation in Central Nervous System Diseases.Molecular neurobiology · 2025Review
- The neuroprotective effects of normobaric oxygen therapy after stroke.CNS neuroscience & therapeutics · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cerebral ischemia/reperfusion (I/R) injury increases blood-brain barrier (BBB) permeability, leading to hemorrhagic transformation and brain edema. Normobaric oxygen (NBO) is a routine clinical treatment strategy for this condition. However, its neuroprotective effects remain controversial. This study investigated the effect of different NBO concentrations on I/R injury and explores the involvement of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the underlying mechanism. A mouse middle cerebral artery occlusion (MCAO) model, and an oxygen and glucose deprivation (OGD) model featuring mouse brain microvascular endothelial cells (ECs) called bEnd.3, were used to investigate the effect of NBO on I/R injury. A reactive oxygen species (ROS) inducer and Nrf2-knockdown by RNA were used to explore whether the Nrf2 pathway mediates the effect of NBO on cerebrovascular ECs. In the early stage of MCAO, 40% O
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