ReviewMolecular neurobiology2025
Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sleep Deprivation, Cytokine Dysregulation, and the Risk of Cardiac Arrhythmia in Dogs.Veterinary medicine and science · 2026Pooled it
- Targeting CD4⁺ T cell infiltration: mechanisms and therapeutic insights into CD4⁺ T cell transmigration across the blood-brain barrier in acute ischemic stroke.Fluids and barriers of the CNS · 2026Review
- G Protein-Coupled Receptors in Cerebrovascular Diseases: Signaling Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Network Pharmacology-Based and Experimental Validation Elucidate the Target Mechanism of Vinorine in Ameliorating Secondary Brain Injury After Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
- JAK inhibitors in livedoid vasculopathy associated with thrombophilia and refractory to anticoagulation: report and literature review.Anais brasileiros de dermatologiaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Cerebrovascular disease (CVD) is a significant neurological condition resulting from pathological changes in the brain's blood supply and is currently the leading cause of death and disability worldwide. The progression of CVD is closely associated with endothelial damage, plaque formation, and thrombosis, driven by long-term alterations in vascular endothelial cells, smooth muscle cells, microglia, and other immune-inflammatory cells. Among the key molecular pathways involved, the Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling pathway plays a central role. Dysregulation of the JAK-STAT pathway is implicated in the pathogenesis of CVD by influencing the aforementioned cell types and associated pathological processes. Importantly, the role of the JAK-STAT pathway varies across different types of CVD and throughout different stages of disease progression (e.g., pre-morbid, acute, and chronic phases). This review examines the composition, activation, and regulation of the JAK-STAT pathway and summarizes recent findings on its involvement in CVD. We discuss the distinct roles of JAK-STAT signaling in various CVD conditions, the potential reasons for these differences, and explore the clinical translational prospects and technical challenges of targeting the JAK-STAT pathway for therapeutic intervention in CVD.
Indexed as
Identifiers
40102347What Socratic 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 Socratic graph.