Mir429 is a member of the miR-200 family, which plays important roles in a variety of biological processes. It is involved in regulating gene expression post-transcriptionally, and is associated with pathways such as epithelial-to-mesenchymal transition (EMT), cell proliferation, and apoptosis. Its dysregulation has implications for many disease conditions, making it an important gene for functional studies [4,7,8].

In renal cell cancer, miR429 expression is significantly higher in patients compared to controls. Overexpressing miR429 in renal cancer cells increases cell proliferation and reduces apoptosis, while knockout of miR429 has the opposite effect, suggesting it plays a role in the pathogenesis of renal cancer and could be a prognostic marker [1].

In gastric cancer, lncRNA PCAT19 acts as an oncogene by competitively binding to miR429 and upregulating DHX9 [2].

In the context of angiotensin II-induced effects in the kidney, down-regulation of miR429 contributes to profibrotic effects, and overexpressing miR429 can reverse these changes, protecting against kidney damage [3].

In a murine model of colitis, miR429 is down-regulated, and it regulates mucin gene expression and secretion by targeting MARCKS, suggesting its potential as an anti-colitis therapy [6].

In endothelial cells of diabetic atherosclerosis mice, hydroxysafflor yellow A inhibits ferroptosis by regulating the miR-429/SLC7A11 axis [5].

In conclusion, Mir429 has diverse functions in different biological processes and disease conditions. Studies using gene knockout or overexpression models in cells and animal models, especially in diseases like renal cancer, gastric cancer, kidney fibrosis, colitis, and diabetic atherosclerosis, have revealed its significant roles in cell proliferation, apoptosis, EMT, and fibrosis. These findings contribute to understanding the molecular mechanisms of these diseases and may provide potential therapeutic targets related to Mir429.