Mrpl23, a mitochondrial ribosomal protein gene, is an essential component for the structural and functional integrity of the mitoribosome complex [1]. Mammalian mitoribosomes have acquired new Mrp genes like Mrpl23 during evolution to compensate for ribosomal RNA loss. The genes encoding these proteins are consistently expressed throughout early embryogenesis with little stage or tissue specificity [1].

In clear-cell renal cell carcinoma (ccRCC), MRPL23 protein expression is significantly lower in tumor tissues compared to normal tissues, while its mRNA levels are elevated. High MRPL23 protein expression is associated with poorer overall survival and is an independent prognostic marker, highlighting its potential role in ccRCC pathogenesis [2]. In addition, in the study of human hematopoietic stem and progenitor cells (HSPCs), HSPCs expressing MRPL23 may contribute to differentiation bias into the myeloid lineage [3]. Also, MRPL23 was identified as one of the genes significantly differentially expressed in the tissue of patients with neuropathic pain compared to controls, suggesting it could be a potential therapeutic target for neuropathic pain [4]. Moreover, in the research of Alzheimer's disease, MRPL23 was revealed as one of the key genes associated with the disease and M1 macrophages [5].

In conclusion, Mrpl23 is crucial for the mitoribosome complex. Its abnormal expression is associated with various diseases such as ccRCC, neuropathic pain, and Alzheimer's disease. The study of Mrpl23 in different disease models helps to understand its role in disease development, providing potential directions for diagnosis and treatment.