Neurocardiac Crosstalk at the Molecular and Cellular Interface: Autonomic Signaling, Inflammatory Pathways, and Neurohormonal Remodeling in the Pathogenesis and Progression of Cardiovascular Disease

The intricate interplay between the nervous system and the heart, termed neurocardiac crosstalk, plays a pivotal role in maintaining cardiovascular homeostasis. Dysregulation of this axis, involving autonomic signaling. inflammatory pathways, and neurohormonal remodeling, contributes significantly to the pathogenesis and progression of cardiovascular diseases (CVDs), including heart failure (HF), myocardial infarction (MI), and arrhythmias. This review synthesizes current evidence on the molecular and cellular mechanisms underlying these interactions, highlighting how sympathetic overactivation, parasympathetic withdrawal, and immune-mediated responses exacerbate cardiac remodeling and dysfunction. Key signaling pathways, such as TLR4/MyD88/NF-KB and P2X7R/NLRP3 inflammasomes, are discussed in the context of neuroimmune modulation. Therapeutic strategies targeting these pathways offer promising avenues for mitigating disease progression. Drawing from preclinical and clinical studies, we emphasize the bidirectional nature of neurocardiac communication and its implications for personalized medicine in CVD management.