Malat1, short for Metastasis-associated lung adenocarcinoma transcript-1, is a highly conserved long non-coding RNA (lncRNA) [1,2,3,4,5,6,7,8,9,10]. It is retained in the nucleus and is abundantly expressed in cells and tissues. Malat1 regulates genes at transcriptional and post-transcriptional levels and is involved in multiple cancer-related pathways such as MAPK/ERK, PI3K/AKT, β-catenin/Wnt, Hippo, VEGF, YAP etc [2]. It has been shown to play a significant role in the development and progression of numerous diseases, especially cancer [1,2,3,4,5,6,7,8,9,10]. Genetic models, like gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying Malat1's functions in vivo.

In a mouse model of myocardial infarction, targeted knockdown of Malat1 in endothelial cells exacerbated oxidative stress, attenuated angiogenesis and microvascular perfusion, and decreased cardiac function. Further studies indicated that Malat1 acts as a competing endogenous RNA for miR-26b-5p and forms a signalling axis with Mfn1 to regulate mitochondrial dynamics and endothelial functions [5]. In chondrocytes, MALAT1 knockdown inhibited cell proliferation, promoted apoptosis, and increased extracellular matrix degradation via the miR-150-5p/AKT3 axis [6].

In conclusion, Malat1 is a crucial lncRNA involved in regulating gene expression and multiple biological processes. Studies using KO/CKO mouse models have revealed its role in diseases such as cardiovascular diseases and osteoarthritis. Understanding Malat1's functions through these models provides insights into disease mechanisms and potential therapeutic targets.