C-X-C motif chemokine ligands (CXCL1/CXCL9) in inflammatory pathways underlying epilepsy-related ventricular remodeling: a mendelian randomization study.

Lanjing Wang, Guiyou Liu, Yongle Wang, Yihan Liu, Jinqiao Liu, Xunming Ji, Sijie Li

Abstract read

In one paragraph

Article in Acta neurologica Belgica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

7 authors.

Lanjing WangNeuro Cardio Vascular Diseases Center, Xuanwu Hospital, Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China.

Guiyou LiuBeijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.

Yongle WangDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.

Yihan LiuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.

Jinqiao LiuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.

Xunming JiNeuro Cardio Vascular Diseases Center, Xuanwu Hospital, Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China.

Sijie LiNeuro Cardio Vascular Diseases Center, Xuanwu Hospital, Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China. lisijie@xwh.ccmu.edu.cn.ORCID http://orcid.org/0000-0002-8329-1186

Funding

National Major Science and Technology Projects of China 2023ZD0505306National Natural Science Foundation of China 82371305Natural Science Foundation of Beijing Municipality Z240021

6 · The paper itself

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.

Indexed as

Chemokine CXCL1Chemokine CXCL9EpilepsyInflammationVentricular RemodelingHumansMendelian Randomization AnalysisChemokine CXCL1Chemokine CXCL9CXCL1 protein, humanCXCL9 protein, humanC-X-C motif chemokine ligandEpilepsyEpileptic heartInflammationMendelian randomizationVentricular remodeling

Identifiers

PMID42213301

DOI10.1016/j.pharmthera.2020.107799

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.