Table_1_Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.pdf

This mini-review summarizes the current evidence for the role of macrophage activation and polarization in inflammation and immune response pertinent to interstitial lung disease, specifically pulmonary fibrosis. In the fibrosing lung, the production and function of inflammatory and fibrogenic mediators involved in the disease development have been reported to be regulated by the effects of polarized M1/M2 macrophage populations. The M1 and M2 macrophage phenotypes were suggested to correspond with the pro-inflammatory and pro-fibrogenic signatures, respectively. These responses towards tissue injury followed by the development and progression of lung fibrosis are further regulated by macrophage-derived microRNAs (miRNAs). Besides cellular miRNAs, extracellular exosomal-miRNAs derived from M2 macrophages have also been proposed to promote the progression of pulmonary fibrosis. In a future perspective, harnessing the noncoding miRNAs with a key role in the macrophage polarization is, therefore, suggested as a promising therapeutic strategy for this debilitating disease.

本微型综述总结了当前关于巨噬细胞激活与极化（macrophage activation and polarization）在与间质性肺疾病（interstitial lung disease, ILD）相关的炎症及免疫应答中所发挥作用的证据，尤其聚焦于肺纤维化（pulmonary fibrosis）。在纤维化肺组织中，已有研究表明，疾病发生发展过程中涉及的炎症与促纤维化介质的产生及功能，均受极化后M1/M2型巨噬细胞群体的调控。现有研究认为，M1型与M2型巨噬细胞表型分别对应促炎与促纤维化的特征谱。这类针对组织损伤、继而引发肺纤维化发生与进展的免疫应答，进一步受巨噬细胞源性微小RNA（microRNAs, miRNAs）的调控。除细胞内微小RNA外，M2巨噬细胞来源的细胞外外泌体微小RNA也被认为可促进肺纤维化进展。在未来展望中，靶向调控在巨噬细胞极化中发挥关键作用的非编码微小RNA（noncoding miRNAs），有望成为治疗这一致残性疾病的极具前景的治疗策略。