Cell‐State‐Dependent Association of Panx1 with Inflammatory Myeloid Responses in Ischemic Stroke

Pannexin 1 (Panx1) participates in ATP release, purinergic signaling, and neuroinflammation, but its cellular context in ischemic stroke remains incompletely defined. We integrated bibliometric analysis with single-cell and bulk transcriptomic analyses to characterize Panx1-associated biological and cellular states. Bibliometric trends showed increasing emphasis on ischemia, inflammation, mitochondrial stress, calcium signaling, and regulated cell death. In GSE174574, Panx1 transcript detection was sparse but more frequent after MCAO than in sham brain and was associated with disease-remodeled myeloid populations, including activated microglial and monocyte/macrophage states. Pseudotime analysis placed Panx1-detected cells along an MCAO-associated myeloid activation structure without a strictly monotonic increase in Panx1 detection. Independent validation in GSE58720 further supported enrichment of Panx1-associated myeloid/stress and inflammatory signatures after MCAO. Together, these findings identify an injury-associated inflammatory/myeloid context for Panx1 in ischemic stroke and provide a basis for future mechanistic investigation.