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肥胖症的挑战与机遇:脂肪细胞在组织纤维化中的作用。

Challenges and opportunities in obesity: the role of adipocytes during tissue fibrosis.

机构信息

Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.

The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.

出版信息

Front Endocrinol (Lausanne). 2024 Apr 15;15:1365156. doi: 10.3389/fendo.2024.1365156. eCollection 2024.

DOI:10.3389/fendo.2024.1365156
PMID:38686209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11056552/
Abstract

Obesity is a chronic disease that affects the energy balance of the whole body. In addition to increasing fat mass, tissue fibrosis occurred in white adipose tissue in obese condition. Fibrosis is the over-activation of fibroblasts leading to excessive accumulation of extracellular matrix, which could be caused by various factors, including the status of adipocytes. The morphology of adipocytes responds rapidly and dynamically to nutrient fluctuations. Adaptive hypertrophy of normal adipocytes protects peripheral organs from damage from lipotoxicity. However, the biological behavior of hypertrophic adipocytes in chronic obesity is abnormally altered. Adipocytes lead to fibrotic remodeling of the extracellular matrix by inducing unresolved chronic inflammation, persistent hypoxia, and increasing myofibroblast numbers. Moreover, adipocyte-induced fibrosis not only restricts the flexible expansion and contraction of adipose tissue but also initiates the development of various diseases through cellular autonomic and paracrine effects. Regarding anti-fibrotic therapy, dysregulated intracellular signaling and epigenetic changes represent potential candidate targets. Thus, modulation of adipocytes may provide potential therapeutic avenues for reversing pathological fibrosis in adipose tissue and achieving the anti-obesity purpose.

摘要

肥胖是一种影响全身能量平衡的慢性疾病。除了增加脂肪量,肥胖状态下白色脂肪组织还会发生组织纤维化。纤维化是成纤维细胞的过度激活导致细胞外基质的过度积累,这可能是由多种因素引起的,包括脂肪细胞的状态。脂肪细胞的形态对营养波动的反应迅速而动态。正常脂肪细胞的适应性肥大可保护外周器官免受脂毒性的损害。然而,慢性肥胖中肥大脂肪细胞的生物学行为发生异常改变。脂肪细胞通过诱导未解决的慢性炎症、持续缺氧和增加肌成纤维细胞数量,导致细胞外基质的纤维性重塑。此外,脂肪细胞诱导的纤维化不仅限制了脂肪组织的灵活扩张和收缩,而且通过细胞自主和旁分泌作用引发各种疾病的发展。关于抗纤维化治疗,失调的细胞内信号和表观遗传变化代表了潜在的候选靶点。因此,调节脂肪细胞可能为逆转脂肪组织的病理性纤维化和实现减肥目的提供潜在的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/a2df1e5678f8/fendo-15-1365156-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/dce3a9a1077e/fendo-15-1365156-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/de53bbd2960d/fendo-15-1365156-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/a2df1e5678f8/fendo-15-1365156-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/dce3a9a1077e/fendo-15-1365156-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/de53bbd2960d/fendo-15-1365156-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8b0/11056552/a2df1e5678f8/fendo-15-1365156-g003.jpg

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