Macrophage M1 regulatory diabetic nephropathy is mediated by m6A methylation modification of lncRNA expression.

Immune and inflammatory responses have been identified to play an important role in diabetic nephropathy (DN) (H. Zhou et al. (2021)). It was found that the part of long non-coding RNA (LncRNA) in nephrosis is related to the negative regulation of MicroRNA (miRNA) (C. Gao et al., 2020), which mechanism is unclear; N6-methyladenosine (m6A) is one of the most common mRNA modifications in eukaryotes (Gu et al. (2020)). m6A has been proved in many works of literature can act on the triple helix structure of RNA-DNA and regulate the relationship between lncRNA and specific DNA sites (Fico et al. (2020); Łoboś and Regulska-Ilow (2021); Xu et al. (2021)). Other studies have shown that m6A methylation modification plays a vital role in developing metabolic diseases such as obesity and type 2 diabetes by regulating glucose and lipid metabolism and immune inflammation. In this study, we performed a subgroup analysis of m6A-modified LncRNA expression in the DN transcriptome dataset (LncRNA high-low expression group); the results showed that the presence of Macrophage M1-related lncRNA (LINC00342, LINC00667, and LNC00963) in the process of m6A methylation recognition and metastasis was indirectly related to the downstream demethylase FTO, at the same time, we analyzed the interaction between m6A and RBM15, which is involved in the immune regulation of macrophage M1, and found that there might be a potential interaction between RBM15 and WTAP, which may play a role in regulating the methylation of lncRNA in macrophage M1, the DN was mediated by macrophage M1 immunoreaction of macrophages.