PDF(Pubmed)
Abstract：
Adipose tissue, an indispensable organ, fulfils the pivotal role of energy storage and metabolism and is instrumental in maintaining the dynamic equilibrium of energy and health of the organism. Adipocyte hypertrophy and adipocyte hyperplasia (adipogenesis) are the two primary mechanisms of fat deposition. Mature adipocytes are obtained by differentiating mesenchymal stem cells into preadipocytes and redifferentiation. However, the mechanisms orchestrating adipogenesis remain unclear. Autophagy, an alternative cell death pathway that sustains intracellular energy homeostasis through the degradation of cellular components, is implicated in regulating adipogenesis. Furthermore, adipose tissue functions as an endocrine organ, producing various cytokines, and certain inflammatory factors, in turn, modulate autophagy and adipogenesis. Additionally, autophagy influences intracellular redox homeostasis by regulating reactive oxygen species, which play pivotal roles in adipogenesis. There is a growing interest in exploring the involvement of autophagy, inflammation, and oxidative stress in adipogenesis. The present manuscript reviews the impact of autophagy, oxidative stress, and inflammation on the regulation of adipogenesis and, for the first time, discusses their interactions during adipogenesis. An integrated analysis of the role of autophagy, inflammation and oxidative stress will contribute to elucidating the mechanisms of adipogenesis and expediting the exploration of molecular targets for treating obesity-related metabolic disorders.
摘要：
脂肪组织,一个不可或缺的器官，发挥能量储存和新陈代谢的关键作用，并有助于维持生物体能量和健康的动态平衡。脂肪细胞肥大和脂肪细胞增生(脂肪生成)是脂肪沉积的两个主要机制。通过将间充质干细胞分化成前脂肪细胞并再分化来获得成熟的脂肪细胞。然而,脂肪生成的机制尚不清楚.自噬,一种替代的细胞死亡途径，通过细胞成分的降解来维持细胞内能量稳态，与调节脂肪生成有关。此外，脂肪组织作为一种内分泌器官,产生各种细胞因子，和某些炎症因子，反过来,调节自噬和脂肪生成。此外,自噬通过调节活性氧影响细胞内氧化还原稳态，在脂肪形成中起关键作用。人们对探索自噬的参与越来越感兴趣，炎症,和脂肪形成中的氧化应激。本手稿回顾了自噬的影响，氧化应激，和炎症对脂肪生成的调节，第一次,讨论了它们在脂肪生成过程中的相互作用。自噬作用的综合分析，炎症和氧化应激将有助于阐明脂肪形成的机制，并加快探索治疗肥胖相关代谢紊乱的分子靶标。
