Neat1, also known as Nuclear paraspeckle assembly transcript 1, is a long noncoding RNA. It is a vital component of paraspeckles, playing a role in their formation and integrity. Neat1 is involved in various biological processes, and its dysregulation is associated with multiple diseases, including different types of cancer, liver-related diseases, type 2 diabetes and its complications, and neurological disorders [4,6-9].

In hepatocellular carcinoma, Neat1 deficiency caused senescence in cultured hepatoma cells and protected against HCC progression in a mouse model, suggesting its role in promoting tumor progression [1]. In atherosclerosis, exercise-mediated down-regulation of Neat1 was shown to mitigate endothelial pyroptosis and delay atherosclerosis, with NEAT1-/-mice used to determine its role [2]. In post-stroke conditions, knockdown of Neat1 in mice significantly alleviated lipid droplet agglomeration and inhibited autophagy, leading to improved cerebral perfusion, reduced brain injury, and increased neurological recovery [3].

In conclusion, Neat1 is crucial in multiple biological processes and disease conditions. Studies using gene knockout (KO) or conditional knockout (CKO) mouse models have revealed its role in promoting tumor progression in hepatocellular carcinoma, its contribution to atherosclerosis development, and its impact on post-stroke outcomes. These findings provide insights into potential therapeutic strategies targeting Neat1 for these diseases.