Eif5a, the eukaryotic translation initiation factor 5A, is an evolutionarily conserved protein. It binds ribosomes to facilitate translation of specific peptide motifs, like those with consecutive prolines [1]. Its activity is also associated with pathways such as nuclear mRNA export, mRNA decay, and importantly, mitochondrial function [1]. It has a crucial role in many cellular processes including proliferation, differentiation, autophagy, and apoptosis [1]. Genetic models, especially KO mouse models, have been valuable in understanding its functions.

In SC-specific eIF5A-knockout mice, depletion of eIF5A in muscle stem cells (SCs) results in impaired muscle regeneration, revealing that the spermidine-eIF5A axis is essential for SC activation via controlling MyoD translation [2]. Also, in mouse and cell culture models of non-alcoholic steatohepatitis (NASH), decreases in Eif5aH lead to lower mitochondrial activity and fatty acid β-oxidation, while spermidine treatment restoring EIF5AH can prevent NASH progression [3].

In conclusion, Eif5a plays a vital role in multiple biological processes. Through model-based research, especially KO mouse models, its significance in muscle stem cell activation and preventing NASH progression has been revealed. Understanding Eif5a can provide insights into the mechanisms of muscle-related diseases and NASH, potentially offering new therapeutic strategies.