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慢性炎症对脂肪组织干细胞分化的调控。

Regulation of stem cell differentiation in adipose tissue by chronic inflammation.

机构信息

Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana, USA.

出版信息

Clin Exp Pharmacol Physiol. 2011 Dec;38(12):872-8. doi: 10.1111/j.1440-1681.2011.05596.x.

Abstract
  1. Recent studies suggest that a local hypoxic response leads to chronic inflammation in the adipose tissue of obese individuals. The adipose tissue hypoxia may reflect a compensatory failure in the local vasculature system in response to obesity. 2. Studies suggest that inflammation stimulates angiogenesis and inhibits adipocyte activities in a feedback manner within the obese adipose tissue. Adipose-derived stem cells (ASC) are able to differentiate into multiple lineages of progenitor cells for adipocytes, endothelial cells, fibroblasts and pericytes. Differentiation of ASC into those progenitors is regulated by the adipose tissue microenvironment. 3. As a major factor in the microenvironment, inflammation may favour ASC differentiation into endothelial cells through the induction of angiogenic factors. At the same time, inflammation inhibits ASC differentiation into adipocytes by suppressing peroxisome proliferator-activated receptor γ activity and the insulin signalling pathway. In this context, inflammation may serve as a signal mediating the competition between adipocytes and endothelial cells for the limited source of ASC. 4. It is a new concept that inflammation mediates signals in the competition between adipocytes and endothelial cells for the limited ASC in obesity. There is a lot of evidence that inflammation promotes endothelial cell differentiation. However, this activity of inflammation remains to be established in adipose tissue. The present article reviews the literature in support of this conclusion.
摘要
  1. 最近的研究表明,局部缺氧反应导致肥胖个体脂肪组织的慢性炎症。脂肪组织缺氧可能反映了肥胖时局部血管系统的代偿失败。

  2. 研究表明,炎症以反馈方式刺激肥胖脂肪组织中的血管生成并抑制脂肪细胞活性。脂肪来源的干细胞(ASC)能够分化为脂肪细胞、内皮细胞、成纤维细胞和周细胞等多种祖细胞系。ASC 向这些祖细胞的分化受脂肪组织微环境的调节。

  3. 作为微环境的主要因素,炎症可能通过诱导血管生成因子促进 ASC 向内皮细胞分化。同时,炎症通过抑制过氧化物酶体增殖物激活受体 γ 活性和胰岛素信号通路来抑制 ASC 向脂肪细胞分化。在这种情况下,炎症可以作为一种信号,介导脂肪细胞和内皮细胞之间对有限 ASC 资源的竞争。

  4. 炎症介导肥胖中脂肪细胞和内皮细胞之间对有限 ASC 的竞争的信号是一个新概念。有大量证据表明炎症促进内皮细胞分化。然而,这种炎症的活性在脂肪组织中尚未得到证实。本文综述了支持这一结论的文献。

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