MIAT has been shown to promote cardiac fibrosis through the MIAT/miR-24/Furin/transforming growth factor (TGF)-beta 1 axis (Qu et al., 2017), promote cardiac hypertrophy through the miR-150/P300 axis (Zhu et al., 2016) and miR-93/TLR4 axis (Li et al., 2018), promote extracellular matrix deposition through the miR-29/COL1A1 and COL3A1 axes (Chuang et al., 2020), and regulate vascular endothelial cell function through the miR-150-5p/VEGF axis (Yan et al., 2015). This evidence concerns the gene COL3A1 and cardiac hypertrophy.