Frrs1, Ferric Chelate Reductase 1, is an enzyme involved in reducing Fe3+ to Fe2+ and participates in the electron transport chain and the tricarboxylic acid (TCA) cycle in mitochondria [2]. It is also associated with trace mineral element transport as its mRNA expression was upregulated in the liver and ileal mucosa of fattening pigs under certain stocking density conditions [6].

In cervical squamous cell carcinoma (CESC), HOXD-AS1 promotes CESC by up-regulating FRRS1 via the transcription factor ELF1. Knockdown of FRRS1 inhibited the proliferation and promoted the apoptosis of cervical cancer cells [1]. In intestinal ischemia injury, overexpression of FRRS1 prevented ischemia-induced iron levels, ROS production, lipid peroxidation, inflammatory responses, and cell death, and its downstream mechanism was related to Hippo signaling [2]. Machine learning prediction also identified FRRS1 as a potential Alzheimer's disease risk gene [3]. Additionally, in bladder cancer, FRRS1 was among the genes whose prognostic features were determined based on cuproptosis-related genes analysis [4]. It was also identified as a potential antigen suitable for glioma mRNA vaccine development [5]. In allergic multimorbidity of asthma, dermatitis, and rhinitis in children and adolescents, FRRS1 was among the eight genes that were consistently overexpressed in all types of multimorbidity [7].

In conclusion, Frrs1 is essential for iron reduction and mitochondrial metabolic processes. Its role in multiple diseases, such as cancer, neurodegenerative diseases, and allergic multimorbidity, has been revealed through various research models. Understanding Frrs1 helps to uncover the mechanisms of these diseases and may provide new directions for treatment strategies.