The Role and Mechanism of Neuron-Immune Crosstalk in Ischemic Heart Disease

Ischemic heart disease remains a leading cause of mortality worldwide, and maladaptive cardiac remodeling after myocardial infarction is a major determinant of heart failure progression. Increasing evidence suggests that the nervous and immune systems interact closely to regulate tissue repair; however, the mechanisms by which neuroimmune communication shapes cardiac remodeling after ischemic injury remain poorly understood. This project aims to investigate the role and mechanisms of neuron–immune crosstalk in ischemic heart disease, with a particular focus on the function of immune cell-derived acetylcholine during cardiac repair. Using genetically modified mouse models, lineage tracing approaches, flow cytometry, single-cell transcriptomic analysis, and molecular validation, we will characterize the dynamics of cholinergic immune responses after MI and identify the downstream cellular targets and signaling pathways involved. The findings from this study will provide new insights into neuroimmune regulation of cardiac regeneration and remodeling, and may reveal novel therapeutic strategies targeting immune-derived neurotransmitter signaling for ischemic heart disease.