Ndufs1, NADH:ubiquinone oxidoreductase core subunit S1, is a key component of mitochondrial complex I. It plays a crucial role in oxidative phosphorylation, facilitating the transfer of electrons from NADH to ubiquinone, thus contributing to ATP production. This process is integral to mitochondrial function and energy metabolism in cells. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions [1,2,4].

In various disease conditions, Ndufs1 has been shown to be significant. In myocardial infarction, its cardiac-specific overexpression alleviates cardiac dysfunction, mitochondrial dysfunction, and apoptosis [1]. In diabetic cardiomyopathy, Akap1 deficiency exacerbates the condition by impeding mitochondrial translocation of Ndufs1, leading to mitochondrial dysfunction and cardiomyocyte apoptosis [2]. In pressure-overload-induced myocardial hypertrophy, Ndufs1 deficiency aggravates mitochondrial membrane potential dysfunction [4]. In gastric cancer, loss of Ndufs1 promotes cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway [3].

In conclusion, Ndufs1 is essential for maintaining normal mitochondrial function and energy metabolism. Through model-based research, especially KO/CKO mouse models, its role in diseases like heart failure, diabetes-related cardiomyopathy, and certain cancers has been revealed. Understanding Ndufs1 provides insights into the underlying mechanisms of these diseases, potentially guiding the development of new therapeutic strategies.