Fam3a, a mitochondrial protein, plays diverse essential functions. It is involved in multiple biological processes and associated with various pathways. For instance, it is related to the regulation of ATP synthesis and release, which in turn activates pathways like P2 receptor-Akt-CREB to influence gene expression. It also participates in processes such as cell differentiation, metabolism, and cell survival, making it of great biological importance. Genetic models, like knockout mouse models, have been crucial in studying its functions [1-10].

In abdominal aortic aneurysm, Fam3a-deficient murine models showed increased aneurysm formation as Fam3a normally maintains well-differentiated vascular smooth muscle cell (VSMC) status by regulating KLF4 ubiquitination [1]. In acute kidney injury, knockout of Fam3a in mice worsened kidney function decline and increased tubular cell pyroptosis, indicating its protective role [2]. In pancreatic α-cells, global Fam3a knockout mice had increased pancreatic and plasma active GLP-1 levels, suggesting its role in regulating α-cell function [3].

In conclusion, Fam3a is essential for maintaining normal physiological functions in various tissues and organs. Model-based research, especially the use of Fam3a KO mouse models, has revealed its significant contributions in disease areas such as abdominal aortic aneurysm, acute kidney injury, and metabolic disorders related to pancreatic cell function. These findings enhance our understanding of disease mechanisms and may provide potential therapeutic targets.