脂肪组织巨噬细胞包括M1型（促炎）和M2型（抗炎）。肥胖时，M2型巨噬细胞向M1型极化促进脂肪组织慢性低度炎症和胰岛素抵抗；相反，冷暴露激活M2型巨噬细胞，诱导健康的米色脂肪形成。因此，探讨脂肪组织巨噬细胞表型转换的触发因素非常重要。赖氨酰氧化酶(Lysyl Oxidase, Lox)是一种分泌性胺氧化酶，具有趋化因子功能。我们发现：脂肪组织Lox是由脂肪细胞合成和分泌，肥胖时表达增加，米色脂肪形成时被抑制。用BAPN(beta-aminopropionitrile) 抑制Lox活性不仅增加米色脂肪形成，同时抑制脂肪组织炎症，而M2/M1比值增加，提示Lox重塑脂肪组织炎症微环境，但具体机制还不清楚。我们将深入研究脂肪细胞来源的Lox如何通过旁分泌机制调控巨噬细胞招募及极化，进而影响脂肪组织炎症微环境和代谢。该研究可为通过转变巨噬细胞表型和功能促进健康脂肪组织形成提供潜在治疗靶点。

Adipose tissue macrophages (ATMs) are divided into classically activated macrophages (M1) and alternatively activated macrophages (M2). ATM phenotype changed from an anti-inflammatory M2 polarized state to a pro-inflammatory M1 state when obesity occurred, which contributed to the chronic low-grade inflammation of obesity and insulin resistance. In contrast, alternative activation of M2 macrophages enhances the formation of healthy beige fat in white adipose tissue. Therefore, it will be necessary to explore triggers that may account for phenotypical switch of ATMs. Lox (Lysyl Oxidase), a secreted amine oxidase, is a potent chemokine inducing migration of varied cell types. Herein, we found that Lox is synthesized and secreted from adipocytes in adipose tissue. Notably, Lox protein is decreased in healthier beige fat and increased in obese adipose tissue. Specific inhibition of Lox activity with BAPN (beta-aminopropionitrile) stimulated the formation of healthier beige fat with adipose tissue inflammation inhibited, suggesting that Lox is a pro-inflammatory factor in adipose tissue. However, the molecular mechanism involved is still unclear. In this study, we are going to explore the function of Lox mediated-crosstalk between adipocytes and macrophages in adipose tissue inflammation and metabolic dysregulation. Our studies will open up new therapeutic targets for shifting macrophage phenotype and function in order to promote adipose tissue health.