Jiang Xiaoying
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 Yanta West Road, Xi'an, Shaanxi, 710061, China.
Pharmacol Rep. 2025 Feb;77(1):21-30. doi: 10.1007/s43440-024-00661-x. Epub 2024 Oct 7.
Fibrosis, characterized by excess accumulation of extracellular matrix components, disrupts normal tissue structure and causes organ dysfunction. Long noncoding RNAs (lncRNAs) are a subset of RNAs longer than 200 nucleotides that are not converted into proteins. The increasing research indicated that lncRNA maternally expressed gene 3 (MEG3) was dysregulated in the pathologic process of fibrosis in several tissues. LncRNA MEG3 was revealed to regulate the expression of target proteins or serve as a miRNAs sponge to control the development of fibrosis, which was involved in NF-ҡB, PI3K/AKT, JAK2/STAT3, Wnt/β-catenin, ERK/p38, and Hh pathway. Importantly, the interference of MEG3 level ameliorated fibrosis. The present review summarized available studies of lncRNA MEG3 in fibrosis, which is helpful for a deeper understanding of the roles of MEG3 in fibrosis.
纤维化的特征是细胞外基质成分过度积累，它会破坏正常组织结构并导致器官功能障碍。长链非编码RNA（lncRNAs）是一类长度超过200个核苷酸且不被转化为蛋白质的RNA。越来越多的研究表明，lncRNA母系表达基因3（MEG3）在多种组织的纤维化病理过程中表达失调。lncRNA MEG3被发现可调节靶蛋白的表达或作为微小RNA（miRNAs）的海绵体来控制纤维化的发展，这一过程涉及核因子-κB（NF-ҡB）、磷脂酰肌醇-3激酶/蛋白激酶B（PI3K/AKT）、Janus激酶2/信号转导子和转录激活子3（JAK2/STAT3）、Wnt/β-连环蛋白、细胞外信号调节激酶/ p38丝裂原活化蛋白激酶（ERK/p38）和刺猬因子（Hh）信号通路。重要的是，干扰MEG3水平可改善纤维化。本综述总结了lncRNA MEG3在纤维化方面的现有研究，这有助于更深入地了解MEG3在纤维化中的作用。
