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N6-Methyladenosine (M6A) is actually a posttranscriptional D4 Receptor site modification identified in eukaryotic messenger RNA (mRNA), which can be equivalent to DNA methylation and histone modification and is regulated by a number of methyltransferases (Bushkin et al., 2019; Gu et al., 2019; Berulava et al., 2020). Methyltransferase complexes are composed of METTL3 (methyltransferase-like three), METTL14 and their more linker molecules like WTAP (Wilms tumor connected protein) andFrontiers in Cell and Developmental Biology | frontiersin.orgNovember 2021 | Volume 9 | ArticleFan et al.m6A Methylation in Liver FibrosisFIGURE 1 | A schematic HDAC7 Formulation 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, as well as the m6A RNA was separated by immunoprecipitation magnetic beads particularly recognizing m6A web pages. Subsequently, the m6A-seq and RNA-seq library were constructed and sequenced.KIAA1429, which can catalyze mRNA m6A methylation. The m6A methylation site on RNA is recognized by m6A-binding proteins, including YTHDC1/2 (1ap2 containing YTH domain), YTHDF1/2/3 (YTH family proteins 1) and IGF2BP1/2/3 (insulin-like development issue two mRNA binding protein 1/2/3), which can bind to methylated m6A internet sites and execute distinct functions. In addition, demethyltransferase FTO (fat mass and obesity related protein) and ALKBH5 (alkyl B homolog 5) reduce 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 approach (Lu et al., 2020). It has been confirmed that m6A modification affects the handle 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 vital roles in a selection 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 many cases of liver injury, which can be 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 could be the most common pathological consequence of liver illnesses and may possibly lead to liver cirrhosis and liver cancer, and in some cases develop into liver failure in extreme situations (Wang Q. et al., 2020). Existing research have found that m6A methylation plays an extremely crucial function within a selection of physiological and pathological processes with the liver (Lin et al., 2020; Ondo et al., 2021). Zhong et al. (2019) identified that the m6A binding protein YTHDF2 can inhibit tumor proliferation and growth by lowering the stability of EGFR mRNA in hepatocellular carcinoma. Ma et al. (2017) found that the methyltransferase METTL14 can inhibit the metastasis of hepatocellular carcinoma by regulating the methylation of microRNAs. Nevertheless, as a preliminary approach in these serious liver illnesses, m6A methylation in LF is rarely described.The purpose of this study was to establish the expression profile of m6A modification in mice with LF and to discover the possible regul