切除Prdm16和色脂肪的身份导致血管重塑和血压升高
Mascha Koenen1, Tobias Becher1,2, Giulia Pagano1
1Laboratory of Molecular Metabolism, The Rockefeller University, New York, NY, USA.
概括
在调节血压方面发挥关键作用. 失去白色脂肪细胞的身份导致高血压,由QSOX1酶介导,突出显示了心血管疾病的新目标.
科学领域:
- 心血管生物学
- 脂肪组织生物学
- 代谢疾病
背景情况:
- 过多的脂肪是高血压和心脏病的重要危险因素.
- 棕色脂肪组织与心血管保护有关,但因果关系尚不清楚.
- 色脂肪是一种可诱导的棕色脂肪,是研究这些效应的相关模型.
研究的目的:
- 研究色脂肪细胞在脂肪细胞与血管交叉交流中的作用.
- 了解色脂肪如何影响血压的机制.
- 识别参与这个过程的分子媒介.
主要方法:
- 使用特定脂肪细胞的Prdm16淘汰小鼠来消除色脂肪细胞的身份.
- 分析周周脂肪组织重塑,血管反应和血压.
- 研究了循环酶QSOX1的表达和作用.
主要成果:
- 导致周周脂肪组织重塑,增加血管反应性和血压升高.
- 在缺乏Prdm16的脂肪细胞中,循环酶QSOX1被上调.
- 在淘汰的小鼠中删除Qsox1改善了血管纤维化和血管反应.
结论:
- 色脂肪细胞是血压的关键调节者.
- QSOX1是脂肪细胞和血管之间的交叉对话的关键媒介.
- 针对QSOX1可能为与脂肪相关的高血压提供治疗潜力.
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