Mir32, a microRNA, is a key regulator of gene expression at the post-transcriptional level [2]. It is involved in multiple biological processes such as cell proliferation, apoptosis, oncogenesis, invasion, metastasis, and drug resistance [2]. Alterations in its expression have been associated with numerous diseases, including metabolic, cardiovascular disorders, and various cancers [2].

In the context of vascular smooth muscle cell (VSMC) calcification, miR32-5p promoted VSMC calcification by upregulating TNFα in the microenvironment. Bioinformatics analysis and experimental verification showed that miR32-5p could target PIKfyve, affecting the production of TNFα in microglia [1].

In the liver, miR-32-5p was found to induce hepatic steatosis and hyperlipidemia by triggering de novo lipogenesis. Hepatocyte-specific miR-32 knockout (miR-32-HKO) ameliorated hepatic steatosis and metabolic disorders in high-fat diet-fed mice, while hepatic miR-32 overexpression exacerbated these abnormalities [3].

In prostate cancer, transgenic overexpression of miR-32 in hiMYC mice increased tumor burden and led to a more aggressive tumor phenotype, and Pdk4 was identified as a tumor-associated miR-32 target [4].

In conclusion, Mir32 plays diverse and significant roles in various biological processes and disease conditions. Studies using gene knockout models, like miR-32-HKO in mice, have revealed its functions in diseases such as vascular calcification, hepatic steatosis, and prostate cancer. These findings contribute to a better understanding of the underlying mechanisms of these diseases and may provide potential therapeutic targets.