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解析肥胖诱导的脂肪组织纤维化的细胞相互作用。

Deciphering the cellular interplays underlying obesity-induced adipose tissue fibrosis.

机构信息

Nutrition and Obesities: Systemic Approaches (NutriOmics, UMRS U1269), INSERM, Sorbonne Université, Paris, France.

Immunometabolism, Department of Nutrition, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

出版信息

J Clin Invest. 2019 Oct 1;129(10):4032-4040. doi: 10.1172/JCI129192.

DOI:10.1172/JCI129192
PMID:31498150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6763252/
Abstract

Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adipose tissue expansion, which is necessary to buffer nutrient excess. Patients with higher visceral fat mass are at a higher risk of developing severe complications such as type 2 diabetes and cardiovascular and liver diseases. However, increased fat mass does not fully explain obesity's propensity to promote metabolic diseases. With chronic obesity, adipose tissue undergoes major remodeling, which can ultimately result in unresolved chronic inflammation leading to fibrosis accumulation. These features drive local tissue damage and initiate and/or maintain multiorgan dysfunction. Here, we review the current understanding of adipose tissue remodeling with a focus on obesity-induced adipose tissue fibrosis and its relevance to clinical manifestations.

摘要

肥胖是由热量摄入和能量消耗之间的失衡引起的,这种失衡会促进脂肪组织的扩张,这对于缓冲营养过剩是必要的。内脏脂肪质量较高的患者发生 2 型糖尿病和心血管及肝脏疾病等严重并发症的风险更高。然而,脂肪质量的增加并不能完全解释肥胖促进代谢疾病的倾向。随着慢性肥胖的发生,脂肪组织会发生重大重塑,最终可能导致无法解决的慢性炎症导致纤维化堆积。这些特征会导致局部组织损伤,并引发和/或维持多器官功能障碍。在这里,我们回顾了目前对脂肪组织重塑的理解,重点介绍了肥胖引起的脂肪组织纤维化及其与临床表现的相关性。

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