ReviewCNS neuroscience & therapeutics2025
Mfsd2a-Targeted Therapy for Ischemic Stroke: Mechanisms, Evidence, and Future Prospects.
Review in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
backgroundIschemic stroke remains a major cause of global disability and mortality, with blood-brain barrier (BBB) dysfunction being a pivotal event in its pathology. Major facilitator superfamily domain-containing 2a (Mfsd2a), a key lipid transporter at the BBB, has emerged as a promising yet underexplored therapeutic target.
objectiveThis review proposes a unifying framework that positions Mfsd2a as a central indicator of ischemic stroke pathophysiology and a potential target for treatment. Although direct clinical evidence remains in its early stages, this review synthesizes foundational knowledge from diverse fields.
methodsWe revisit the established biological functions of Mfsd2a, including its role in inhibiting caveolae-mediated transcytosis and transporting omega-3 fatty acids, and detail its core mechanisms in maintaining BBB integrity. This review also correlates these functions with their significant downregulation following ischemic stroke. We then critically evaluate the limited but compelling preclinical evidence from models in which Mfsd2a has been directly targeted and explore innovative therapeutic strategies. Finally, we explicitly address the current limitations, including the scarcity of direct intervention studies, and outline a translational roadmap for future research.
resultsBy integrating this dispersed evidence chain, this review aims to solidify the theoretical foundation for Mfsd2a-targeted therapies and accelerate their clinical development.
conclusionTargeting Mfsd2a shows a promising therapeutic strategy to protect the BBB and improve neurological outcomes after ischemic stroke.
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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 Socratic graph.