Eissa Mousa G, Artlett Carol M
Department of Microbiology & Immunology, Drexel University College of Medicine, Drexel University, 2900 Queen Lane, Philadelphia, PA 19129, USA.
Noncoding RNA. 2019 Mar 12;5(1):23. doi: 10.3390/ncrna5010023.
The function of microRNAs (miRNAs) during fibrosis and the downstream regulation of gene expression by these miRNAs have become of great biological interest. miR-155 is consistently upregulated in fibrotic disorders, and its ablation downregulates collagen synthesis. Studies demonstrate the integral role of miR-155 in fibrosis, as it mediates TGF-β1 signaling to drive collagen synthesis. In this review, we summarize recent findings on the association between miR-155 and fibrotic disorders. We discuss the cross-signaling between macrophages and fibroblasts that orchestrates the upregulation of collagen synthesis mediated by miR-155. As miR-155 is involved in the activation of the innate and adaptive immune systems, specific targeting of miR-155 in pathologic cells that make excessive collagen could be a viable option before the depletion of miR-155 becomes an attractive antifibrotic approach.
微小RNA（miRNA）在纤维化过程中的功能以及这些miRNA对基因表达的下游调控已成为生物学研究的热点。miR-155在纤维化疾病中持续上调，其缺失可下调胶原蛋白的合成。研究表明miR-155在纤维化中起重要作用，因为它介导转化生长因子-β1信号传导以驱动胶原蛋白合成。在本综述中，我们总结了关于miR-155与纤维化疾病关联的最新研究结果。我们讨论了巨噬细胞和成纤维细胞之间的交叉信号传导，这种信号传导协调了由miR-155介导的胶原蛋白合成上调。由于miR-155参与先天和适应性免疫系统的激活，在miR-155缺失成为一种有吸引力的抗纤维化方法之前，特异性靶向产生过多胶原蛋白的病理细胞中的miR-155可能是一种可行的选择。
