Epicardial adipose tissue (EAT) has the unique property to release mediators that nourish the heart in healthy conditions, an effect that becomes detrimental when volume expands and proinflammatory cytokines start to be produced. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a proinflammatory mediator involved in atherosclerosis, is also produced by visceral fat. Due to the correlation of inflammation with PCSK9 and EAT enlargement, we evaluated whether PCSK9 was expressed in EAT and associated with EAT inflammation and volume. EAT samples were isolated during surgery. EAT thickness was measured by echocardiography. A microarray was used to explore EAT transcriptoma. The PCSK9 protein levels were measured by Western Blot in EAT and ELISA in plasma. PCSK9 was expressed at both the gene and protein levels in EAT. We found a positive association with EAT thickness and local proinflammatory mediators, in particular, chemokines for monocytes and lymphocytes. No association was found with the circulating PCSK9 level. The expression of PCSK9 in EAT argues that PCSK9 is part of the EAT secretome and EAT inflammation is associated with local PCSK9 expression, regardless of circulating PCSK9 levels. Whether reducing EAT inflammation or PCSK9 local levels may have beneficial effects on EAT metabolism and cardiovascular risk needs further investigations.

中文翻译：

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PCSK9 在心外膜脂肪组织中的表达：与局部组织炎症的分子关联。


心外膜脂肪组织 (EAT) 具有独特的特性，可以释放在健康条件下滋养心脏的介质，当体积扩大并开始产生促炎细胞因子时，这种作用就会变得有害。前蛋白转化酶枯草杆菌蛋白酶/kexin 9 型 (PCSK9) 是一种参与动脉粥样硬化的促炎介质，也是由内脏脂肪产生的。由于炎症与 PCSK9 和 EAT 增大的相关性，我们评估了 PCSK9 是否在 EAT 中表达以及与 EAT 炎症和体积相关。手术期间分离了 EAT 样本。通过超声心动图测量 EAT 厚度。使用微阵列来探索 EAT 转录瘤。通过 EAT 中的蛋白质印迹和血浆中的 ELISA 测量 PCSK9 蛋白水平。 PCSK9 在 EAT 中在基因和蛋白质水平上都有表达。我们发现 EAT 厚度和局部促炎介质，特别是单核细胞和淋巴细胞的趋化因子呈正相关。未发现与循环 PCSK9 水平相关。 PCSK9 在 EAT 中的表达表明 PCSK9 是 EAT 分泌组的一部分，并且 EAT 炎症与局部 PCSK9 表达相关，无论循环 PCSK9 水平如何。减少 EAT 炎症或 PCSK9 局部水平是否可能对 EAT 代谢和心血管风险产生有益影响，需要进一步研究。