Depression aggravates myocardial infarction via an adenosine-mediated brain-heart signaling pathway that activates microglia and systemic inflammation, a process that can be mitigated by fluoxetine.
This study provides molecular evidence that depression exacerbates myocardial injury via elevated habenular adenosine, which triggers neuroinflammation and subsequent systemic inflammation leading to cardiomyocyte death.
抑郁不仅影响心理状态，还会引发全身性生理改变。流行病学证据显示，抑郁显著增加急性心肌梗死的发生风险并加重不良预后，但其内在机制尚不明确。本研究基于化学探针策略，构建基于核酸适配体的荧光纳米探针，实现了活体脑内小分子腺苷的实时成像，发现抑郁状态下情绪相关的缰核区域腺苷水平异常升高。进一步研究表明，腺苷可激活脑内免疫细胞并诱导神经炎症反应，继而触发全身性炎症过程，促进心肌细胞死亡，从而加重心肌损伤。该工作为阐明情绪障碍与心血管疾病之间的内在联系提供了分子层面的证据。
Zhang et al. (Fri,) conducted a editorial in Depression and Myocardial Infarction. Depression vs. No depression was evaluated on Myocardial injury and brain adenosine levels. Depression aggravates myocardial infarction via an adenosine-mediated brain-heart signaling pathway that activates microglia and systemic inflammation, a process that can be mitigated by fluoxetine.