异常的脂肪细胞枯死巨噬细胞的极性和功能与反复自发流产（RSA）密切相关。C1q/肿瘤坏死因子相关蛋白6（CTRP6）是脂肪素寡聚体家族的成员，对炎症、葡萄糖摄取和肿瘤转移起着不可或缺的作用。然而，CTRP6对RSA中巨噬细胞极性和糖酵解的调节作用以及其潜在机制尚未完全阐明。在本研究中，我们首先通过双重免疫荧光分析发现CTRP6的表达与M1巨噬细胞标记物（CD86）在滋养组织中呈正相关。体外实验表明，CTRP6可以通过PPAR-γ/NF-κB通路促进M1巨噬细胞的活化，并操控巨噬细胞的糖酵解。值得注意的是，除了沉默CTRP6外，PPAR-γ激动剂（GW1929）的治疗还抑制了M1巨噬细胞的极化，并在体内恢复了胚胎吸收。综上所述，这些结果揭示了CTRP6在RSA期间巨噬细胞转化中的以往未知功能。版权©2023 Elsevier B.V.保留所有权利。

Aberrant polarization and functions of decidual macrophages are closely related to recurrent spontaneous abortion (RSA). C1q/tumor necrosis factor-related protein 6 (CTRP6) is a member of the adiponectin paralog family, and plays indispensable roles in inflammation, glucose uptake and tumor metastasis. However, the regulatory effect of CTRP6 on macrophage polarization and glycolysis in RSA and the underlying mechanisms have not been fully elucidated. In the present study, we first found that CTRP6 expression was positively correlated with the M1 macrophage marker (CD86) in decidual tissues by dual immunofluorescence analysis. In vitro experiments indicated that CTRP6 could facilitate M1 macrophage activation through the PPAR-γ/NF-κB pathway and manipulate the glycolysis of macrophages. Notably, in addition to silencing CTRP6, treatment with a PPAR-γ agonist (GW1929) inhibited M1 macrophage polarization and rescued embryo absorption in vivo. Taken together, these results identify previously unrevealed functions of CTRP6 in macrophage transformation during RSA.Copyright © 2023 Elsevier B.V. All rights reserved.