Fis1-flox Mouse

Fis1, short for mitochondrial fission 1 protein, is a key outer mitochondrial membrane protein crucial for mitochondrial fission. It is involved in the recruitment of the mitochondrial fission GTPase dynamin-related protein-1 (Drp1) to mitochondria, which is essential for the process of mitochondrial division. This process is vital for maintaining mitochondrial function, and thus, overall cellular homeostasis. Mitochondrial fission, regulated by Fis1, also has implications in many biological processes such as cell apoptosis, metabolism, and organelle network regulation [1,2,3].

In various disease models, Fis1 has been shown to play significant roles. In septic cardiomyopathy, the interaction between Drp1 and Fis1 leads to mitochondrial dysfunction, and inhibiting this interaction using P110 can reduce oxidative stress and cardiac dysfunction [1]. In hepatocellular carcinoma, Met-mediated phosphorylation of Fis1 at Tyr38 promotes mitochondrial fission, which in turn facilitates cell metastasis [2]. In acute kidney injury, renal ischemia-reperfusion injury causes mitochondrial fragmentation through Drp1-Fis1 interaction, and P110, which disrupts this interaction, can alleviate the injury [4].

In conclusion, Fis1 is essential for mitochondrial fission and maintaining cellular function. Studies using models like gene-targeted manipulations in mice have revealed its significance in diseases such as septic cardiomyopathy, hepatocellular carcinoma, and acute kidney injury. Understanding the role of Fis1 in these disease conditions may provide potential therapeutic targets for treatment.