The incidence of heart failure after myocardial infarction (MI) remains high and the underlying causes are incompletely understood. The crosstalk between heart and adipose tissue and stimulated lipolysis has been identified as potential driver of heart failure. Lipolysis is also activated acutely in response to MI. However, the role in the post-ischemic remodeling process and the contribution of different depots of adipose tissue is unclear. Here, we employ a mouse model of 60 min cardiac ischemia and reperfusion (I/R) to monitor morphology, cellular infiltrates and gene expression of visceral and subcutaneous white adipose tissue depots (VAT and SAT) for up to 28 days post ischemia. We found that in SAT but not VAT, adipocyte size gradually decreased over the course of reperfusion and that these changes were associated with upregulation of UCP1 protein, indicating white adipocyte conversion to the so-called ‘brown-in-white’ phenotype. While this phenomenon is generally associated with beneficial metabolic consequences, its role in the context of MI is unknown. We further measured decreased lipogenesis in SAT together with enhanced infiltration of MAC-2⁺ macrophages. Finally, quantitative PCR analysis revealed transient downregulation of the adipokines adiponectin, leptin and resistin in SAT. While adiponectin and leptin have been shown to be cardioprotective, the role of resistin after MI needs further investigation. Importantly, all significant changes were identified in SAT, while VAT was largely unaffected by MI. We conclude that targeted interference with lipolysis in SAT may be a promising approach to promote cardiac healing after ischemia.

心肌梗死 (MI) 后心力衰竭的发生率仍然很高，其根本原因尚不完全清楚。心脏和脂肪组织之间的串扰以及刺激的脂肪分解已被确定为心力衰竭的潜在驱动因素。脂解作用也被急性激活以响应 MI。然而，在缺血后重塑过程中的作用以及不同脂肪组织库的贡献尚不清楚。在这里，我们使用 60 分钟心脏缺血和再灌注 (I/R) 的小鼠模型来监测缺血后长达 28 天的内脏和皮下白色脂肪组织库（VAT 和 SAT）的形态学、细胞浸润和基因表达。我们发现在 SAT 而不是 VAT 中，脂肪细胞的大小在再灌注过程中逐渐减小，并且这些变化与 UCP1 蛋白的上调有关，表明白色脂肪细胞转化为所谓的“白色棕色”表型。虽然这种现象通常与有益的代谢结果相关，但它在 MI 中的作用尚不清楚。我们进一步测量了 SAT 中脂肪生成的减少以及 MAC-2 的浸润增强⁺巨噬细胞。最后，定量 PCR 分析揭示了 SAT 中脂肪因子脂联素、瘦素和抵抗素的瞬时下调。虽然脂联素和瘦素已被证明具有心脏保护作用，但心肌梗死后抵抗素的作用需要进一步研究。重要的是，所有重大变化都在 SAT 中确定，而增值税在很大程度上不受 MI 的影响。我们得出结论，靶向干扰 SAT 中的脂肪分解可能是促进缺血后心脏愈合的一种有前途的方法。