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N6-Methyladenosine (M6A) is really a posttranscriptional modification found in eukaryotic messenger RNA (mRNA), which is related to DNA methylation and histone modification and is regulated by a variety of methyltransferases (Bushkin et al., 2019; Gu et al., 2019; Berulava et al., 2020). Methyltransferase complexes are composed of METTL3 (methyltransferase-like 3), METTL14 and their extra linker molecules including WTAP (Wilms tumor related protein) andFrontiers in Cell and Developmental Biology | frontiersin.orgNovember 2021 | Volume 9 | ArticleFan et al.m6A Methylation in Liver FibrosisFIGURE 1 | A schematic diagram of m6A-seq and RNA-seq analyses of mice with LF. LF was induced by subcutaneous injection of CCl4 in mice, and extracted total RNA from liver. Then, RNA was fragmented, and also the m6A RNA was separated by immunoprecipitation magnetic beads especially recognizing m6A sites. Subsequently, the m6A-seq and RNA-seq library have been constructed and sequenced.KIAA1429, which can catalyze mRNA m6A methylation. The m6A methylation internet site on RNA is recognized by m6A-binding proteins, such as YTHDC1/2 (1ap2 containing YTH domain), YTHDF1/2/3 (YTH family members proteins 1) and IGF2BP1/2/3 (insulin-like development aspect 2 mRNA binding protein 1/2/3), which can bind to methylated m6A internet sites and execute particular functions. Furthermore, demethyltransferase FTO (fat mass and obesity related protein) and ALKBH5 (alkyl B homolog five) lessen m6A modified RNA to original RNA (Du et al., 2018; Zhang Z. et al., 2020; Mapperley et al., 2021). The combined action of those methyltransferases tends to make m6A modification a dynamic and reversible method (Lu et al., 2020). It has been confirmed that m6A modification affects the manage of key cellular processes, such as RNA stability (Wang et al., 2014), translation efficiency (Wang et al., 2015), secondary structure (Liu et al., 2015), subcellular localization (Meyer and Jaffrey, 2014), splicing and transport (Yang et al., 2018), and plays significant roles in a assortment of illnesses (Zhang B. et al., 2020; Liu et al., 2020). Liver fibrosis (LF) is defined as excessive deposition of extracellular matrix (ECM) in response to several circumstances of liver injury, which is a reversible abnormal tissue response, and excessive activation of hepatic stellate cells (HSCs) is central to its pathogenesis (Bataller and Brenner, 2005; Zhang et al., 2017; Smith-Cortinez et al., 2020). LF would be the most typical pathological consequence of liver ailments and may well cause liver cirrhosis and liver cancer, as well as create into liver failure in severe situations (Wang Q. et al., 2020). Current Kainate Receptor Compound studies have discovered that m6A methylation plays an exceptionally vital function within a variety of physiological and pathological processes from the liver (Lin et al., 2020; Ondo et al., 2021). Zhong et al. (2019) located that the m6A binding protein YTHDF2 can inhibit tumor proliferation and development by minimizing the stability of EGFR mRNA in hepatocellular carcinoma. Ma et al. (2017) located that the methyltransferase METTL14 can inhibit the metastasis of hepatocellular carcinoma by regulating the methylation of microRNAs. On the other hand, as a preliminary course of action in these severe liver illnesses, m6A methylation in LF is seldom described.The purpose of this study was to establish the expression profile of m6A modification in mice with LF and to explore the possible regul