ArticleInternational journal of molecular sciences2019
Lipid Reshaping and Lipophagy Are Induced in a Modeled Ischemia-Reperfusion Injury of Blood Brain Barrier.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Rat brain phospholipid remodeling correlates with plasma lipid clearance and late functional vulnerability after ischemic stroke.iScience · 2026Article
- Autophagy in ischemic stroke: from cellular survival mechanism to pathological damage.Metabolic brain disease · 2026Review
- Ferroptosis and Its Crosstalk with Other Cell Death Modes in Ischemic Stroke.Current medicinal chemistry · 2026Review
- The link between ferroptosis and autophagy in myocardial ischemia/reperfusion injury: new directions for therapy.Journal of cardiovascular translational research · 2025Review
- Lipidomic analysis identifies long-chain acylcarnitine as a target for ischemic stroke.Journal of advanced research · 2024Article
- Potential relationship between autophagy and ferroptosis in myocardial ischemia/reperfusion injury.Genes & diseases · 2023Review
- Reinventing the Penumbra - the Emerging Clockwork of a Multi-modal Mechanistic Paradigm.Translational stroke research · 2023Review
- Lipidomic signature of stroke recurrence after transient ischemic attack.Scientific reports · 2023Article
- Inhibition of ERK downregulates autophagy via mitigating mitochondrial fragmentation to protect SH-SY5Y cells from OGD/R injury.Cell communication and signaling : CCS · 2023Article
- The regulatory role of lipophagy in central nervous system diseases.Cell death discovery · 2023Review
- Article
- Cell Death Mechanisms in Cerebral Ischemia-Reperfusion Injury.Neurochemical research · 2022Review
- NMMHC IIA triggered lipid metabolize reprogramming resulting in vascular endothelial cellular tight junction injury.Molecular biology reports · 2022Article
- Coffee-Derived Phenolic Compounds Activate Nrf2 Antioxidant Pathway in I/R Injury In Vitro Model: A Nutritional Approach Preventing Age Related-Damages.Molecules (Basel, Switzerland) · 2022Article
- Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Crosstalk Between Autophagy and Ferroptosis and Its Putative Role in Ischemic Stroke.Frontiers in cellular neuroscience · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic-reperfusion (I/R) injury induced a remodeling of protein and lipid homeostasis, under oxidative stress and inflammatory status. Starvation occurring during I/R is a condition leading to autophagy activation, which allows abnormal material clearance or amino acid, or both, and fatty acid (FA) recycling essential for survival. This study investigated the lipid reshaping, peroxidation, and related-signaling pathways, in rat brain endothelial cells (RBE4) subjected to 3 h of oxygen and glucose deprivation (OGD) and restoration of standard condition (I/R in vitro model). Lipids and proteins were analyzed after 1 or 24 h of oxygen and nutrient restoration. Together with the oxidative stress and inflammatory status, I/R injury induced a reshaping of neutral lipids and biogenesis of lipid droplets (LD) with excessive lipid storage. The increase of LC3-II/LC3-I ratio, an autophagy marker, and LC3 co-localization with LD suggest the activation of lipophagy machinery to counteract the cell engulfment. Lipophagy leads to cholesterol ester (CE) hydrolysis, increasing free cholesterol (FC) secretion, which occurred by specific transporters or unconventional exocytosis pathways, or both. Here, we propose that an unconventional spreading of FC and other lipid metabolites may influence the neurovascular unit (NVU) cells, contributing to Blood brain barrier (BBB) alteration or adaptation, or both, to the cumulative effects of several transient ischemia.
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