Adipose is a key tissue regulating energy homeostasis. In states of obesity, caloric intake exceeds energy expenditure, thereby accelerating lipid accumulation with ongoing extracellular matrix (ECM) remodeling. Excess deposition of lipids and expansion of adipocytes potentially decrease ECM flexibility with local hypoxia and inflammation. Hypoxia and chronic low-grade inflammation accelerate the development of adipose tissue fibrosis and related metabolic dysfunctions. Adipose tissue remodeling impacts localized adipose tissue metabolism, which including adipogenesis, angiogenesis, insulin sensitivity, cytokine secretion profile, and in turn alters systemic glucose and lipid homeostasis. The activation and maintenance of beige adipocyte is a potential therapeutic strategy for combating HFD-induced adipose tissue fibrosis and insulin resistance. In this review, we focused on the regulatory mechanisms and mediators in remodeling of adipose tissue fibrosis, along with their relevance to clinical manifestations.

中文翻译：

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Mini-Review：对抗脂肪组织重塑中的纤维化

脂肪是调节能量稳态的关键组织。在肥胖状态下，热量摄入超过能量消耗，从而通过正在进行的细胞外基质 (ECM) 重塑加速脂质积累。脂质的过量沉积和脂肪细胞的扩张可能会降低 ECM 的灵活性，并伴有局部缺氧和炎症。缺氧和慢性低度炎症加速脂肪组织纤维化和相关代谢功能障碍的发展。脂肪组织重塑影响局部脂肪组织代谢，包括脂肪生成、血管生成、胰岛素敏感性、细胞因子分泌谱，进而改变全身葡萄糖和脂质稳态。米色脂肪细胞的激活和维持是对抗 HFD 诱导的脂肪组织纤维化和胰岛素抵抗的潜在治疗策略。