Plexin C1 during Myocardial Ischemia Reperfusion Injury

• Applicants: Professor Dr. Michael Köppen; Professor Dr. Peter Rosenberger
• Subject Area: Anaesthesiology ; Immunology ; Cardiology, Angiology
• Term: since 2025
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 562291681

Myocardial infarction remains a leading cause of mortality worldwide, with reperfusion paradoxically exacerbating tissue damage by up to 50%. Reperfusion injury is marked by an intensified inflammatory response, prominently involving neutrophils and monocytes. Emerging evidence suggests that neuronal guidance cues, particularly Plexin C1, play a crucial role in regulating inflammatory processes. Plexin C1 is a transmembrane receptor that modulates immune cell adhesion and migration, potentially mitigating inflammatory damage. Preliminary studies indicate that Plexin C1 is upregulated during myocardial ischemia-reperfusion and exerts protective effects. Plexin C1 deficiency exacerbates tissue injury, inflammatory cytokine release, and thromboinflammatory complex formation. This project aims to elucidate the molecular mechanisms of Plexin C1 in myocardial ischemia-reperfusion injury and explore potential therapeutic strategies. Specifically, we will (1) analyze Plexin C1 expression and activation in myocardial tissue, (2) investigate its role in regulating immune cell dynamics, and (3) evaluate therapeutic interventions such as agonists or antibodies targeting Plexin C1. Our findings aim to pave the way for innovative treatments to mitigate myocardial injury.

• DFG Programme: Research Grants