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The entry "Adenosine receptor and Vascular Endothelial Growth Factor (VEGF) expression" refers to a signaling axis rather than a single molecular target. **Adenosine receptors** (primarily subtypes A2A and A2B) are G protein-coupled receptors that, when activated by adenosine, stimulate the transcription and secretion of **VEGF**, a potent endothelial cell cytokine and key regulator of angiogenesis[1][2][3][5]. This interaction is central to tissue repair, inflammation, and tumor growth. Agonists targeting these receptors have been shown to upregulate VEGF via cAMP-PKA-CREB and PI3K-AKT pathways, with A2B playing a prominent role in human endothelial cells[2]. VEGF biomarkers and plasma levels indicate functional activation of this axis. While pharmacological modulation holds promise for tissue regeneration and repair, caution is warranted, as excess VEGF or angiogenesis can contribute to pathological states, including cancer progression and vascular-related complications[2][7]. **Because this target merges two distinct biological entities and does not correspond to a single druggable protein or gene, it is not a valid molecular target in standard therapeutic or biomarker databases.**
Adenosine receptor agonists (A2A/A2B activation upregulates VEGF via cAMP/PKA/CREB and PI3K/AKT-mediated signaling); Adenosine uptake inhibition (raises extracellular adenosine to stimulate VEGF); VEGF inhibitors (inhibit VEGF-VEGF receptor interaction, block downstream angiogenic effects).
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