Blockade of mesenteric and omental adipose tissue sensory neurons improves cardiac remodeling through sympathetic pathway

MI model was established by ligation of the left anterior descending coronary artery in SD rats. Two weeks post-MI, RNA-seq transcriptome sequencing of MOAT indicated significant changes in genes related to signal transduction and the endocrine system, including adiponectin and lipolysis- and inflammatory-related genes, potentially influenced afferent activity. Then MI model followed by microinjection of capsaicin (CAP) was used to block the MOAT sensory afferent nerves. Two weeks later, MOAT sensory nerve denervation (CAP group) significantly prevented cardiac remodeling and improved cardiac function as measured by echocardiography. Heart rate variability (HRV) analysis revealed that CAP recovered the cardiac sympathetic nerve hyperactivation and cardiac autonomic imbalance after MI, accompanied by reduced serum norepinephrine. In addition, the calcitonin gene-related peptide (CGRP) expression was enhanced in dorsal root ganglion (DRG) indicating elevated afferent flow post-MI. The neuron activity marker c-fos was overexpressed in the hypothalamic paraventricular nucleus (PVN) and superior cervical ganglion (SCG), suggesting an enhanced efferent flow of the brain-heart sympathetic axis. The increased intensity of TH and ChAT compared to the Sham group illustrated the neurochemical remodeling of SCG neurons. These changes were rectified by CAP.