PDF(Pubmed)
Abstract：
UNASSIGNED: Myocardial infarction (MI) is the primary cause of death in subjects with type 2 diabetes (T2D) and their in-hospital mortality after MI is still elevated compared with those without T2D. Therefore, it is of crucial importance to identify possible mechanisms of worse clinical outcomes and mortality in T2D subjects. Monocyte/macrophage-mediated immune response plays an important role in heart remodelling to limit functional deterioration after MI. Indeed, first pro-inflammatory macrophages digest damaged tissue, then anti-inflammatory macrophages become prevalent and promote tissue repair. Here, we hypothesize that the worse clinical outcomes in patients with T2D could be the consequence of a defective or a delayed polarization of macrophages toward an anti-inflammatory phenotype.
UNASSIGNED: In an exploratory human study, circulating monocytes from male patients with or without T2D at different time-points after MI were in vitro differentiated toward pro- or anti-inflammatory macrophages. The results of this pilot study suggest that the phenotype of circulating monocytes, as well as the pro- and anti-inflammatory macrophage polarization, or the kinetics of the pro- and anti-inflammatory polarization, is not influenced by T2D.
UNASSIGNED: Further studies will be necessary to understand the real contribution of macrophages after MI in humans.
UNASSIGNED: In an exploratory human study, circulating monocytes from male patients with or without T2D at different time-points after MI were in vitro differentiated toward pro- or anti-inflammatory macrophages. The results of this pilot study suggest that the phenotype of circulating monocytes, as well as the pro- and anti-inflammatory macrophage polarization, or the kinetics of the pro- and anti-inflammatory polarization, is not influenced by T2D.
UNASSIGNED: Further studies will be necessary to understand the real contribution of macrophages after MI in humans.
摘要：
■心肌梗塞（MI）是2型糖尿病（T2D）患者的主要死亡原因，与没有T2D的患者相比，MI后的住院死亡率仍然升高。因此,确定T2D受试者临床结局和死亡率较差的可能机制至关重要.单核细胞/巨噬细胞介导的免疫反应在心脏重塑中起重要作用，以限制MI后的功能恶化。的确,首先，促炎巨噬细胞消化受损组织，然后抗炎巨噬细胞变得普遍并促进组织修复。这里,我们假设T2D患者更差的临床结局可能是巨噬细胞向抗炎表型极化缺陷或延迟的结果.
■在一项探索性人类研究中，在MI后不同时间点,来自有或无T2D的男性患者的循环单核细胞在体外分化为促炎或抗炎巨噬细胞.这项初步研究的结果表明，循环单核细胞的表型，以及促炎和抗炎的巨噬细胞极化，或者促炎和抗炎极化的动力学，不受T2D的影响。
■需要进一步的研究来了解人MI后巨噬细胞的真正贡献。
■在一项探索性人类研究中，在MI后不同时间点,来自有或无T2D的男性患者的循环单核细胞在体外分化为促炎或抗炎巨噬细胞.这项初步研究的结果表明，循环单核细胞的表型，以及促炎和抗炎的巨噬细胞极化，或者促炎和抗炎极化的动力学，不受T2D的影响。
■需要进一步的研究来了解人MI后巨噬细胞的真正贡献。
