Mrpl12, also known as mitochondrial ribosomal protein L7/L12, is a member of the mitochondrial ribosomal proteins. It plays a crucial role in mitochondrial metabolism, with potential involvement in mitochondrial transcription regulation [1-5, 8]. It is essential for maintaining mitochondrial homeostasis and is likely part of pathways related to metabolic reprogramming and mitochondrial biogenesis [1,2]. Genetic models, such as mouse models, have been valuable in studying its functions.

In lung adenocarcinoma (LUAD) mouse models (Tp53fl/fl;KrasG12D-driven), deletion of Mrpl12 conferred a survival advantage, delaying tumor onset and reducing malignant progression. Mechanistically, Mrpl12 promotes tumor progression by upregulating mitochondrial oxidative phosphorylation, and UBASH3B-mediated dephosphorylation of tyrosine 60 in Mrpl12 inhibits its oncogenic functions [1]. In hepatocellular carcinoma (HCC), Mrpl12 overexpression promoted cell proliferation, migration, invasion, and tumorigenicity in vivo, while knockdown had the opposite effects, and it was found to be crucial for maintaining mitochondrial homeostasis [2]. In acute kidney injury, Mrpl12 specifically binds to adenosine nucleotide translocase 3 (ANT3) under normal conditions, and its decreased expression during AKI leads to abnormal opening of mitochondrial permeability transition pore (MPTP) and cell apoptosis, with overexpression protecting renal tubular epithelial cells (TECs) [3].

In conclusion, Mrpl12 is vital for mitochondrial metabolism and homeostasis. Through gene knockout and conditional knockout mouse models, its role in diseases like LUAD, HCC, and AKI has been revealed. These models have provided insights into how Mrpl12 dysregulation can contribute to disease pathogenesis, suggesting it as a potential therapeutic target for these diseases [1,2,3].