Lin28a is an RNA-binding protein. Initially discovered in Caenorhabditis elegans, it regulates stem cell differentiation and proliferation. In mammals, it plays roles in cell cycle, growth, tissue repair, and metabolism (notably glucose metabolism) through let-7-dependent (binding to let-7) or independent (binding directly to mature mRNA) pathways [1].

In mouse models, LIN28a overexpression in postnatal cardiomyocytes decreased maturation-associated polyploidization, enhanced cell cycle activity, and improved cardiac function after injury, indicating its role in cardiac repair [2]. Conditional ablation and induction of Lin28a + MuSCs in adult mice showed that these cells are crucial for efficient muscle regeneration, suggesting Lin28a connects embryonic factors to adult stem cell self-renewal [3]. Also, in a mouse model of unilateral ureteral obstruction, decreased Lin28a expression was associated with increased renal fibrosis, and overexpression of Lin28a inhibited renal fibrotic markers [4].

In conclusion, Lin28a is essential for multiple biological processes such as stem cell regulation, cardiac repair, muscle regeneration, and renal fibrosis prevention. Studies using KO/CKO mouse models have revealed its significant roles in these areas, providing valuable insights into related disease mechanisms.