Autonomic innervation of the heart plays a pivotal role not only in regulating the heart rate but also in modulating the cardiac cell microenvironment via cell-cell interactions and influencing the heart's repair capabilities. Currently, the primary clinical approach for treating myocardial infarction (MI) is percutaneous coronary intervention. However, the myocardial salvage rate remains low for patients with advanced disease. MI is recognized as an autonomic nervous system disorder, marked by sympathetic hyperactivity and the loss of parasympathetic nerves. Following MI, ventricular sympathetic nerve sprouting occurs, leading to an increase in ventricular sympathetic innervation and, consequently, an increased risk of ventricular arrhythmia, which is the primary cause of sudden cardiac death in patients with a history of MI. The vagus nerve positively regulates cardiomyocyte proliferation and regeneration, enhancing ventricular remodeling and cardiac function post-MI. This process is highly significant in the treatment and rehabilitation of MI. Cardiac autonomic nerves are influenced by factors such as inflammation, immunity, intercellular communication, metabolism, genetics, epigenetics, and cytokine secretion related to cardiac mesenchymal nerves. In recent years, significant advancements have been made regarding treatment for MI, specifically in the fields of autonomic nervous system therapies, stem cell and extracellular vesicle treatments, traditional Chinese medicine acupuncture and moxibustion, and peripheral electrophysiological stimulation and bioengineering materials. The balance of dominance between the sympathetic and parasympathetic nervous systems in the heart affects tissue regeneration and cardiac remodeling after MI. The secretion of neurons regulates the microenvironment of cardiac repair. The neural therapy of MI involves multiple fields such as traditional Chinese medicine, biomaterials, stem cell therapy, and drug research and development, and has broad development prospects Key Messages: The regulation exerted by the cardiac autonomic nervous system on the heart significantly influences the prognosis of MI. This involves nervous system modulation of inflammation and heart rate and complex interactions between neurons and cardiomyocytes, immune cells, fibroblasts, adipocytes, stem cells, and other cellular components. Genetic and epigenetic modifications, as well as shifts in energy metabolism, also play crucial roles.
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