Adipose tissue senescence is a precursor to organismal aging and understanding adipose remodelling contributes to discovering novel anti-aging targets. Glutathione peroxidase 3 (GPx3), a critical endogenous antioxidant enzyme, is diminished in the subcutaneous adipose tissue (sWAT) with white adipose expansion. Based on the active role of the antioxidant system in counteracting aging, we investigated the involvement of GPx3 in adipose senescence. We determined that knockdown of GPx3 in adipose tissue by adeno-associated viruses impaired mitochondrial function in mice, increased susceptibility to obesity, and exacerbated adipose tissue senescence. Impairment of GPx3 may cause mitochondrial dysfunction through inner mitochondrial membrane disruption. Adipose reshaping management (cold stimulation and intermittent diet) counteracted the aging of tissues, with an increase in GPx3 expression. Overall metabolic improvement induced by cold stimulation was partially attenuated when GPx3 was depleted. GPx3 may be involved in adipose browning by interacting with UCP1, and GPx3 may be a limiting factor for intracellular reactive oxygen species (ROS) accumulation during stem cell browning. Collectively, these findings emphasise the importance of restoring the imbalanced redox state in adipose tissue to counteract aging and that GPx3 may be a potential target for maintaining mitochondrial homeostasis and longevity.

中文翻译：

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谷胱甘肽过氧化物酶 3 通过维持线粒体稳态来对抗脂肪重塑中的衰老至关重要


脂肪组织衰老是生物体衰老的前兆，了解脂肪重塑有助于发现新的抗衰老靶点。谷胱甘肽过氧化物酶 3 （GPx3） 是一种关键的内源性抗氧化酶，在皮下脂肪组织 （sWAT） 中随着白色脂肪的扩张而减少。基于抗氧化系统在对抗衰老中的积极作用，我们研究了 GPx3 与脂肪衰老的关系。我们确定腺相关病毒敲低脂肪组织中 GPx3 会损害小鼠的线粒体功能，增加肥胖的易感性，并加剧脂肪组织衰老。GPx3 损伤可能通过线粒体内膜破坏导致线粒体功能障碍。脂肪重塑管理 （冷刺激和间歇性饮食） 抵消了组织的衰老，增加了 GPx3 表达。当 GPx3 耗尽时，冷刺激诱导的总体代谢改善部分减弱。GPx3 可能通过与 UCP1 相互作用参与脂肪褐变，GPx3 可能是干细胞褐变过程中细胞内活性氧 （ROS） 积累的限制因素。总的来说，这些发现强调了恢复脂肪组织中不平衡的氧化还原状态以对抗衰老的重要性，并且 GPx3 可能是维持线粒体稳态和长寿的潜在靶标。