Adipose inflammation is an important cause for obesity-associated metabolic disorders, including insulin resistance and hypertension. Here we investigated that a circular RNA (circRNA), which we termed circARF3 (ADP-ribosylation factor 3), acts as an endogenous miR-103 sponge to alleviate adipose inflammation by promoting mitophagy. On the other hand, miR-103 aggravated inflammation by inhibiting mitophagy, revealing that miR-103 acts as a positive regulator of adipose inflammation. Furthermore, we found that tumor necrosis factor receptor-associated factor 3 (TRAF3), as a miR-103 downstream target, mediates the functions of miR-103 in adipose inflammation. Overexpressing TRAF3 attenuated miR-103-induced inflammation by accelerating mitophagy. Moreover, we identified that circARF3 blocked miR-103 effects, which resulted in an increase in TRAF3 expression. TRAF3 restrained the nuclear factor κB (NF-κB)-signaling pathway, heightened mitophagy, and suppressed NLRP3 inflammasome activation ultimately. Our data showed that circARF3 acts as an endogenous miR-103 sponge to inhibit mitophagy-mediated adipose inflammation both in vitro and in vivo. These findings disclose a new regulatory pathway for adipose inflammation, which consists of circARF3, miR-103, and TRAF3. This study can be a useful addition to our knowledge, as it provides a new strategy for the prevention of adipose inflammation in obesity disorder.

脂肪炎症是与肥胖相关的代谢紊乱的重要原因，包括胰岛素抵抗和高血压。在这里，我们研究了一种环状RNA（circRNA），我们将其称为circARF3（ADP-核糖基化因子3），作为内源性miR-103海绵，通过促进线粒体吞噬减轻脂肪炎症。另一方面，miR-103通过抑制线粒体吞噬而加剧了炎症，表明miR-103充当了脂肪炎症的正调节剂。此外，我们发现作为miR-103下游靶标的肿瘤坏死因子受体相关因子3（TRAF3）介导miR-103在脂肪炎症中的功能。过表达TRAF3可以通过加速线粒体吞噬来减轻miR-103诱导的炎症。此外，我们发现circARF3阻断了miR-103的作用，导致TRAF3表达增加。TRAF3抑制核因子κB（NF-κB）信号通路，增强线粒体吞噬，并最终抑制NLRP3炎性体的激活。我们的数据表明，circARF3可以作为内源性miR-103海绵来抑制线粒体介导的脂肪炎症体外和体内。这些发现揭示了一种新的脂肪炎症调节途径，该途径由circARF3，miR-103和TRAF3组成。这项研究可以为我们的知识提供有用的补充，因为它为预防肥胖症中的脂肪炎症提供了新的策略。