ArticleScientific reports2025
Upregulation of VEGFA through the adenosine A2A receptor is a crucial pathway for inhibiting pericyte apoptosis in chronic cerebral hypoperfusion.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Microglia-Mediated Vascular Network Remodeling After Ischemic Stroke: An Immunovascular Repair Framework.Cells · 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
3 authors.
Funding
Abstract
Chronic cerebral hypoperfusion (CCH) is a key factor in vascular cognitive impairment. Pericyte loss and subsequent blood-brain barrier disruption play pivotal roles in the pathogenesis of CCH-induced white matter lesions (CCH-WMLs). Previous work suggested that the adenosine A2A receptor (A2AR) may protect pericytes in CCH-WMLs, but the mechanisms are not fully understood. In this study, we induced CCH in Sprague‒Dawley rats via bilateral carotid artery occlusion and treated them with the A2AR agonist CGS21680 or the A2AR antagonist SCH58261. Our findings revealed that CGS21680 significantly inhibited the expression of the proapoptotic proteins BAX and Caspase 3, while SCH58261 obviously promoted it. The expression of the antiapoptotic protein Bcl-2 was markedly increased by CGS21680 in OGD-exposed pericytes. Additionally, the expression of the transcription factors Rap-1, ERK, and phosphorylated ERK also increased dramatically in OGD-exposed pericytes following CGS21680 administration. VEGFA and VEGFR2 expression was upregulated by CGS21680 and downregulated by SCH58261 in pericytes after OGD. Furthermore, VEGFA knockdown via a shRNA-expressing adenovirus counteracted the protective effect of A2AR against pericyte apoptosis following OGD. Notably, the expression of BAX and Caspase3 was significantly upregulated, and the expression of BCL-2 was markedly downregulated in OGD-exposed pericytes after Rap-1 knockdown via a shRNA-expressing adenovirus. Rap-1 suppression obviously reduced the levels of phosphorylated ERK, VEGFA and VEGFR2 in pericytes, suggesting a role for the Rap1-ERK pathway in the A2AR-induced upregulation of VEGFA expression. Overall, A2AR activation inhibits pericyte apoptosis and may exert neuroprotective effects against CCH by increasing VEGFA expression through the Rap1-ERK signaling pathway.
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.