Huang Jiaxing, Liu Xinyu, Qiu Qinfang, Tan Wuping, Li Rui, Xi Haosong, Peng Chen, Zhou Liping, Zhou Xiaoya, Wang Yueyi, Jiang Hong
Department of Cardiology, Renmin Hospital of Wuhan University; Hubei Key Laboratory of Autonomic Nervous System Modulation; Taikang Center for Life and Medical Sciences, Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, P.R. China.
iScience. 2024 Jun 18;27(7):110245. doi: 10.1016/j.isci.2024.110245. eCollection 2024 Jul 19.
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 (), neuropeptide Y (), and complement 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.
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进行通信，并通过传入信号间接与中枢神经系统进行通信。心肌梗死（MI）可能会诱发MOAT的病理改变，进而影响心脏功能。我们的研究表明，MI会导致MOAT中与信号转导相关的基因发生显著转录变化，包括脂联素（）、神经肽Y（）和补体C3（），这可能会影响传入活动。我们进一步发现，用辣椒素（CAP）对MOAT感觉神经进行去神经支配可预防心脏重塑，改善心脏功能，并逆转MI组心脏交感神经的过度激活，同时血清去甲肾上腺素水平降低。此外，CAP可逆转MI后MOAT传入输入增加和脑-心交感神经输出增加的情况，增加脂联素（APN）和神经肽Y（NPY），降低补体C3（C3）和血清促炎因子。这些结果表明，阻断MOAT传入感觉神经可通过抑制脑-心交感神经轴发挥心脏保护作用。
