PDF(Pubmed)
Abstract：
Mesenteric and omental adipose tissue (MOAT) communicates directly with the heart through the secretion of bioactive molecules and indirectly through afferent signaling to the central nervous system. Myocardial infarction (MI) may induce pathological alterations in MOAT, which further affects cardiac function. Our study revealed that MI induced significant MOAT transcriptional changes in genes related with signal transduction, including adiponectin (APN), neuropeptide Y (NPY), and complement C3 (C3), potentially influencing afferent activity. We further found that MOAT sensory nerve denervation with capsaicin (CAP) prevented cardiac remodeling, improved cardiac function, and reversed cardiac sympathetic nerve hyperactivation in the MI group, accompanied by reduced serum norepinephrine. In addition, CAP reversed the elevated MOAT afferent input and brain-heart sympathetic outflow post-MI, increasing APN and NPY and decreasing C3 and serum proinflammatory factors. These results demonstrated that blockade of the MOAT afferent sensory nerve exerts a cardioprotective effect by inhibiting the brain-heart sympathetic axis.
摘要：
肠系膜和网膜脂肪组织（MOAT）通过生物活性分子的分泌直接与心脏通信，并通过传入信号传导到中枢神经系统间接地与心脏通信。心肌梗死（MI）可能导致MOAT的病理改变，这进一步影响心脏功能。我们的研究表明，MI诱导与信号转导相关的基因发生显著的MOAT转录变化，包括脂联素（APN），神经肽Y（NPY），和补码C3（C3），潜在影响传入活动。我们进一步发现，MOAT感觉神经神经与辣椒素（CAP）预防心脏重塑，改善心脏功能，并逆转MI组的心脏交感神经过度激活，伴有血清去甲肾上腺素降低。此外,CAP逆转了MI后升高的MOAT传入输入和脑心交感神经流出，增加APN和NPY，降低C3和血清促炎因子。这些结果表明，MOAT传入感觉神经的阻断通过抑制脑-心脏交感神经轴来发挥心脏保护作用。
