Role of Cx43 and ACKR3 in Modulating Astrocytic Response and Neuronal Survival Post-Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a devastating neurological disorder that results from the accumulation of blood in the brain's subarachnoid space, leading to significant challenges in neurological recovery. This study explores the molecular interactions between Connexin 43 (Cx43) and Atypical Chemokine Receptor 3 (ACKR3) in astrocytes following SAH, with a focus on their roles in neuroinflammation and neuronal Apoptosis. Through transcriptome Sequencing and a range of functional assays, we have identified crucial alterations in astrocytic gene expression triggered by the modulation of these proteins. Our results indicate that the Cx43-ACKR3 axis plays a pivotal role in exacerbating neuroinflammatory responses and enhancing neuronal Apoptosis, which are key contributors to the pathology of SAH. The data reveal that disrupting this axis could serve as a therapeutic target, suggesting potential interventions to mitigate neuroinflammation, restore astrocytic functionality, and ultimately protect against neuronal damage. This study contributes to the understanding of glial cell dynamics in SAH and opens avenues for novel therapeutic approaches to treat this severe condition.

Cx43‐mediated gap junctions; astrocytes; inflammatory processes; neurological condition; subarachnoid hemorrhage; transcriptome sequencing.