Autonomic nervous system dysfunction, characterized by sympathovagal imbalance, plays a significant role in irritable bowel syndrome pathophysiology and represents a potential therapeutic target.
This review highlights the role of sympathovagal imbalance in IBS pathophysiology and identifies autonomic circuits as potential therapeutic targets.
This review synthesizes current evidence on autonomic nervous system (ANS) dysfunction in irritable bowel syndrome (IBS). Patients with IBS often exhibit sympathovagal imbalance–reduced vagal tone with relative sympathetic hyperactivity–which correlates with symptom severity and shows subtype specificity. The ANS orchestrates bidirectional brain–gut communication via interactions with psychosocial factors, low-grade neuroinflammation, and the gut microbiota. Key mechanisms include vagal afferent signaling by microbial metabolites, sympathetic regulation of mucosal immunity, stress-induced disruption of autonomic homeostasis, and neuroplastic changes in intestinal and central pain pathways. Emerging evidence supports therapeutic targeting of autonomic circuits through vagus nerve stimulation, pharmacological modulation of serotonin and adrenergic receptors, and microbiome-based interventions. Current challenges include methodological limitations in assessing neural dynamics and insufficient integration of multi-system interactions. Future research should employ multi-omics approaches to elucidate pathway-specific mechanisms and develop precision medicine strategies for this heterogeneous disorder.
Bai et al. (Thu,) conducted a review in Irritable bowel syndrome. Autonomic nervous system dysfunction, characterized by sympathovagal imbalance, plays a significant role in irritable bowel syndrome pathophysiology and represents a potential therapeutic target.