Intercellular Communication Pathways in Cerebral Ischemia: Mechanisms, Molecular Insights, and Therapeutic Implications.

Introduction: Cerebral ischemia (CI) is a severe neurological disorder characterized by high incidence and disability rates. Its pathogenesis is complex, involving multiple interrelated biological processes. Among these, intercellular communication has emerged as a key mechanism regulating the damage and recovery phases of CI. It controls information exchange between cells, thereby playing a crucial role in cellular responses to ischemic injury. Understanding how intercellular communication promotes the pathophysiology of CI may provide valuable insights into new therapeutic targets.

Methods: To elucidate the role of intercellular communication in CI, recent literature was analyzed, with a focus on how intercellular communication influences cellular behaviors and metabolism. This review integrates data from molecular biology, cellular signaling studies, and cerebral ischemia models.

Results: Studies indicate that intercellular communication significantly influences the progression and outcomes of CI. Intercellular communication not only participates in regulating the inflammatory response following injury but also plays a dual role in neuroprotection and regeneration.

Discussion: The dual role of intercellular communication-exacerbating damage through inflammatory cascades and promoting recovery through neuroprotective mechanisms-highlights its complex contribution to the pathology of CI. Cellular crosstalk between neurons, glial cells, endothelial cells, and immune cells coordinates the dynamic response to ischemic injury. Understanding these dynamics offers promising opportunities for targeted interventions.

Conclusion: Intercellular communication plays a central role in the mechanisms of injury and repair in cerebral ischemia. By influencing inflammation, neuroprotection, and regeneration, it serves as both a mediator of injury and a potential therapeutic target. Further research is needed to fully elucidate these mechanisms and translate them into effective clinical strategies for treating CI.