Frrs1, or Ferric Chelate Reductase 1, is an enzyme involved in the reduction of Fe3+ to Fe2+ and is associated with the electron transport chain and the tricarboxylic acid (TCA) cycle in mitochondria [2].

In cervical squamous cell carcinoma (CESC), the lncRNA HOXD-AS1 promotes CESC by up-regulating FRRS1 via the transcription factor ELF1. Transfection of sh-FRRS1 inhibited the proliferation and promoted the apoptosis of SiHa and Hela 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 and tau-based screening identified FRRS1 as a potential Alzheimer's disease risk gene [3]. In bladder cancer, the prognostic features of FRRS1 were determined through the analysis of cuproptosis-related genes, and the CRG molecular typing and risk scores were correlated with various clinicopathological features [4]. FRRS1 was also identified as a potential antigen suitable for glioma mRNA vaccine development [5]. In fattening pigs, stocking density affected the mRNA expression of FRRS1, which is related to trace mineral element deposition and transport [6]. Additionally, FRRS1 was among the genes overexpressed in multimorbidity of asthma, dermatitis, and rhinitis in children and adolescents [7].

In summary, Frrs1 is involved in multiple biological processes and diseases. Its role in cancer development, ferroptosis-mediated intestinal ischemia injury, Alzheimer's disease, and allergic multimorbidity, among others, highlights its importance. Research on Frrs1 using various models helps in understanding the underlying molecular mechanisms, potentially providing new insights for disease treatment and prevention.