Mir32, a microRNA, is a group of endogenous, small noncoding RNA molecules that function by base-pairing with the mRNA of genes and regulating gene expression at the post-transcriptional level [2]. It has been implicated in various biological processes such as cell proliferation, apoptosis, oncogenesis, invasion, metastasis, drug resistance, and is also involved in metabolic and cardiovascular disorders [2].

In the context of vascular smooth muscle cell (VSMC) calcification, miR32-5p promoted VSMC calcification by upregulating TNFα in the microenvironment. Bioinformatics analysis was used to identify TNFα as a candidate inflammatory factor associated with calcification. miR32-5p mimic treatment increased TNFα expression, while miR32-5p antagomir treatment decreased it. PIKfyve was identified as a candidate target gene of miR32-5p, and rescue experiments further supported the role of miR32-5p in this process [1].

In hepatic lipid metabolism, miR-32-5p was found to induce hepatic steatosis and hyperlipidemia by triggering de novo lipogenesis. Hepatocyte-specific miR-32 knockout (miR-32-HKO) in high-fat diet-fed mice ameliorated hepatic steatosis and metabolic disorders, 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 miR-32 was shown to regulate the prostate secretome and identify Pdk4 as a tumor-associated target [4].

In summary, Mir32 plays diverse and crucial roles in different biological processes and disease conditions. Studies using gene knockout or overexpression models in mice have revealed its functions in vascular calcification, hepatic lipid metabolism, and prostate cancer. These findings contribute to understanding the underlying mechanisms of related diseases and may provide potential therapeutic targets for treatment.