MIAT, short for Myocardial Infarction Associated Transcript, is a nuclear long non-coding RNA (lncRNA) longer than 200 nucleotides. It acts as a competitive endogenous RNA (ceRNA), interacting with microRNAs (miRNAs) to regulate post-transcriptional processes, thus influencing protein expression [1]. MIAT is involved in multiple cellular and molecular processes and is of great biological importance in various pathological conditions.

In the context of diseases, knockdown of lncRNA Miat alleviates pirarubicin-induced cardiotoxicity by regulating miR-129-1-3p in immortalized mouse cardiomyocytes [2]. In diabetic retinopathy, exosomal lncRNA-MIAT promotes neovascularization via the miR-133a-3p/MMP-X1 axis, and reducing its level mitigates retinal neovascularization in a mouse model of oxygen-induced retinopathy [3]. Also, in LPS-induced J774A.1 macrophages, silencing MIAT increases inflammatory cytokines and impedes autophagy, while MIAT functions as a ceRNA, sponging miR-30a-5p to regulate SOCS1, suggesting its potential as a therapeutic target for rheumatoid arthritis inflammation [4].

In conclusion, MIAT plays crucial roles in various non-oncological pathological conditions such as cardiovascular diseases, autoimmune diseases, and diabetic complications. Through model-based research, especially knockdown experiments in cell and mouse models, we have gained insights into its functions in disease-related biological processes. These findings offer potential directions for the development of diagnostic, prognostic, and therapeutic strategies targeting MIAT-related pathways.