Exosomal miR-34a: the code for adipocyte-macrophage communication

Xiao Han, Yaqin Zhang
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Abstract

The study “ Adipocyte-secreted exosomal microRNA-34a inhibits M2 macrophage polarization to promote obesity-induced adipose inflammation ”, presented by Pan et al . and published in J Clin Invest, has been read by us with great interest (1). In this study, the authors uncovered adipocyte-secreted exosomes as a potentially novel mediator of obesity-induced adipose inflammation, acting by transporting miR-34a into the adjacent macrophages, where it drives the polarization program toward proinflammatory M1 phenotype by targeting the transcription factor KLF4. Indeed, this study provided a new question for obesity-induced systemic inflammation and metabolic dysregulation, but in terms of the molecular mechanism of miR-34a on M1/M2 polarization, there still are something to clarify and need for more investigation.
外泌体miR-34a:脂肪细胞-巨噬细胞通讯的编码
Pan等人提出的研究“脂肪细胞分泌的外泌体微小RNA-34a抑制M2巨噬细胞极化以促进肥胖诱导的脂肪炎症”。并发表在《临床投资杂志》上,被我们饶有兴趣地阅读(1)。在这项研究中,作者发现脂肪细胞分泌的外泌体是肥胖诱导的脂肪炎症的一种潜在的新介质,它通过将miR-34a转运到邻近的巨噬细胞中发挥作用,在巨噬细胞中,它通过靶向转录因子KLF4来驱动促炎M1表型的极化程序。事实上,这项研究为肥胖诱导的全身炎症和代谢失调提供了一个新的问题,但就miR-34a对M1/M2极化的分子机制而言,仍有一些需要澄清的地方,需要更多的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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