ReviewCells2024
AIBP: A New Safeguard against Glaucomatous Neuroinflammation.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- The Dual Role of Macroglia in Glaucoma: Deciphering the Contributions of Astrocytes and Müller Cells to Retinal Neurodegeneration and Neuroprotection.International journal of molecular sciences · 2026Review
- Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026Review
- AIBP deficiency drives MAFLD advancement via ITGβ3 mediated lipid metabolism disruption and pro-inflammatory activation.Cell communication and signaling : CCS · 2026Article
- Toll-Like Receptors in Diabetes: Immunometabolic Mechanisms and Emerging Precision Therapeutic Strategies.Journal of inflammation research · 2026Review
- Restoring AIBP expression in the retina provides neuroprotection in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Exosomes in Regulating miRNAs for Biomarkers of Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Amyloid β-Induced Inflammarafts in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Apolipoprotein A-I binding protein-mediated neuroprotection in glaucomatous neuroinflammation and neurodegeneration.Neural regeneration research · 2025Article
- Lipid rafts: novel therapeutic targets for metabolic, neurodegenerative, oncological, and cardiovascular diseases.Lipids in health and disease · 2025Review
- Glial-mediated immune modulation in glaucomatous neurodegeneration: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Association between systemic inflammatory response index and glaucoma incidence from 2005 to 2008.Frontiers in medicine · 2025Article
- The role of RGC degeneration in the pathogenesis of glaucoma.International journal of biological sciences · 2025Review
- AIBP Protects Müller Glial Cells Against Oxidative Stress-Induced Mitochondrial Dysfunction and Reduces Retinal Neuroinflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Integrated Bioinformatics-Based Identification and Validation of Neuroinflammation-Related Hub Genes in Primary Open-Angle Glaucoma.International journal of molecular sciences · 2024Article
- Apolipoprotein A-I: Potential Protection Against Intestinal Injury Induced by Dietary Lipid.Journal of inflammation research · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Glaucoma is a group of ocular diseases that cause irreversible blindness. It is characterized by multifactorial degeneration of the optic nerve axons and retinal ganglion cells (RGCs), resulting in the loss of vision. Major components of glaucoma pathogenesis include glia-driven neuroinflammation and impairment of mitochondrial dynamics and bioenergetics, leading to retinal neurodegeneration. In this review article, we summarize current evidence for the emerging role of apolipoprotein A-I binding protein (AIBP) as an important anti-inflammatory and neuroprotective factor in the retina. Due to its association with toll-like receptor 4 (TLR4), extracellular AIBP selectively removes excess cholesterol from the plasma membrane of inflammatory and activated cells. This results in the reduced expression of TLR4-associated, cholesterol-rich lipid rafts and the inhibition of downstream inflammatory signaling. Intracellular AIBP is localized to mitochondria and modulates mitophagy through the ubiquitination of mitofusins 1 and 2. Importantly, elevated intraocular pressure induces AIBP deficiency in mouse models and in human glaucomatous retina. AIBP deficiency leads to the activation of TLR4 in Müller glia, triggering mitochondrial dysfunction in both RGCs and Müller glia, and compromising visual function in a mouse model. Conversely, restoring AIBP expression in the retina reduces neuroinflammation, prevents RGCs death, and protects visual function. These results provide new insight into the mechanism of AIBP function in the retina and suggest a therapeutic potential for restoring retinal AIBP expression in the treatment of glaucoma.
Indexed as
Identifiers
What OpenQuestion holds
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.