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C-X-C motif chemokine ligands (CXCL1/CXCL9) in inflammatory pathways underlying epilepsy-related ventricular
Lanjing Wang1,2, Guiyou Liu3, Yongle Wang2
1Neuro Cardio Vascular Diseases Center, Xuanwu Hospital, Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China.
Insights
Epilepsy causally impacts heart structure and function, with inflammation playing a key role. Specific inflammatory proteins, CXCL1 and CXCL9, mediate these cardiac changes, particularly ventricular remodeling.
Area of Science:
- Cardiology
- Neurology
- Genetics
- Immunology
Background:
- Cardiac abnormalities are frequently observed in epilepsy patients.
- The precise mechanisms linking epilepsy and cardiac dysfunction are not fully understood.
- Inflammation is a suspected mediator in the epilepsy-heart connection.
Purpose of the Study:
- To investigate epilepsy-related structural and functional cardiac alterations.
- To assess the mediating role of inflammation in epilepsy-induced cardiac changes using a genetic approach.
- To identify specific inflammatory pathways involved in epilepsy-cardiac interplay.
Main Methods:
- A two-step Mendelian randomization (MR) analysis was employed.
- Epilepsy and its subtypes were used as exposures.
- 82 cardiac traits and 91 plasma inflammatory proteins were analyzed as outcomes and mediators, respectively.
Main Results:
- Mendelian randomization confirmed causal relationships between epilepsy (and generalized epilepsy) and cardiac traits.
- Epilepsy and its subtypes were found to causally alter plasma inflammatory protein levels.
- C-X-C motif chemokine ligand (CXCL) 1 and CXCL9 were identified as mediators for epilepsy's effect on left ventricular wall thickness.
Conclusions:
- Epilepsy exerts significant causal effects on cardiac structure and function.
- Inflammation, particularly involving CXCL1 and CXCL9, is a key mechanism mediating epilepsy-related cardiac remodeling.
- These findings highlight potential therapeutic targets for managing cardiac complications in epilepsy.
Abstract:
While cardiac abnormalities are well-documented in epilepsy patients, the underlying mechanisms mediating epilepsy-heart interplay remain incompletely understood. This study aimed to investigate epilepsy- related structural and functional cardiac alterations, and to assess the potential mediating role of inflammation from a genetic standpoint. We conducted a two-step Mendelian randomization (MR) analysis in this study, with epilepsy and its two subtypes (generalized epilepsy and focal epilepsy) as exposures, 82 cardiac traits (76 cardiac phenotypes based on cardiac magnetic resonance imaging and 6 electrocardiogram - based characteristics) as outcomes, as well as 91 plasma inflammatory proteins as mediators. The MR results demonstrated causal correlations of epilepsy and generalized epilepsy on cardiac traits. Epilepsy and its two subtypes can causally induce alterations in plasma inflammatory protein levels. Mediation analysis identified C-X-C motif chemokine ligand (CXCL) 1 and CXCL9 as potential mediators of epilepsy's effect on regional end-diastolic left ventricular wall thickness, accounting for 9.3%~10.0% and 9.1% of the total effects, respectively. In conclusion, epilepsy exhibited significant causal effects on cardiac structure and function, with inflammation potentially serving as a key mediating mechanism. Specifically, CXCL1 and CXCL9 may participate in inflammatory pathways associated with epilepsy-related ventricular remodeling.
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