Miga1, a mammalian homolog of the mitoguardin gene, encodes a mitochondrial outer membrane protein. It is crucial for mitochondrial fusion, a process that maintains mitochondrial morphology and function. Miga1 is involved in pathways such as the Hippo-YAP1 signaling pathway and may collaborate with protein kinase B (AKT) [1]. It also plays a role in processes related to cell metabolism and is important for normal cellular functions. Genetic models, like knockout mouse models, are valuable tools for studying Miga1's function.

In Miga1 knockout mouse models, female mice were found to be subfertile. The ovarian phenotypes indicated that Miga1 plays an important role in ovulation and ovarian steroidogenesis. In Miga1-knockout granulosa cells, there were severe defects in luteinization and steroidogenesis, along with disordered mitochondrial morphology and function in response to gonadotropins [3]. In differentiated adipocytes, down-regulation of Miga1 led to mitochondrial dysfunction, with lower oxygen consumption and decreased UCP1 expression, suggesting its role in adipocyte function and potentially fat distribution [2,4].

In conclusion, Miga1 is essential for maintaining mitochondrial function, which is crucial for processes like ovarian endocrine functions and adipocyte function. The use of Miga1 knockout mouse models has revealed its significance in subfertility-related issues and potentially in diseases related to abnormal fat distribution. These findings contribute to our understanding of the molecular pathogenesis of reproductive endocrine diseases and metabolic disorders.