Pum2, also known as PUMILIO2, is an RNA-binding protein that controls target mRNA turnover and translation by binding to target mRNAs in a sequence-specific manner [2,3]. It is involved in various biological processes and associated with multiple pathways, playing a significant role in maintaining cellular homeostasis. Genetic models, such as gene knockout mouse models, have been crucial in studying its functions.

In a mouse model of acute ischemic kidney injury, genetic deletion of Mff (regulated by Pum2) attenuated ischemic acute kidney injury-induced renal failure, and overexpression of Pum2 reduced Mff upregulation and protected renal tubules [4]. Intestine-specific knockout of Pum2 (along with Pum1) in mice significantly inhibited the progression of colitis-associated cancer in the AOM/DSS model [5]. Knockdown of Pum2 in neonatal rat ventricular cardiomyocytes decreased caspase 3-associated apoptosis under hypoxia/reoxygenation treatment [2]. In an Ang-II-induced aortic dissection mouse model, overexpression of Pum2 impeded the development of aortic dissection [1]. Also, downregulation of Pum2 in mesenchymal stem cells (MSCs) enhanced their osteogenic potential, and in an OVX mouse model, AAV9-siPum2 was a potential gene therapy for osteoporosis [3].

In conclusion, Pum2 is essential in multiple biological processes. Through model-based research, especially KO/CKO mouse models, it has been revealed that Pum2 plays roles in diseases such as acute ischemic kidney injury, colitis-associated cancer, hypoxia/reoxygenation-induced cardiomyocyte injury, thoracic aortic dissection, and osteoporosis. Understanding Pum2's functions provides insights into the underlying mechanisms of these diseases and potential therapeutic targets.