Nup93, a crucial structural protein of the nuclear pore complex (NPC), mediates nucleocytoplasmic transport of transcription factors, playing a vital role in maintaining endothelial health, gene expression regulation, and cell cycle processes [1,2]. It is also associated with various pathways such as the Hippo signaling pathway (Yap-Yes-associated protein) [1]. Genetic models, especially knockout models, are valuable for studying its functions.

In endothelial cells, loss of Nup93 in aged mice and in vitro models of endothelial aging impairs NPC transport, leading to nuclear accumulation of Yap and downstream inflammation, suggesting a role in endothelial cell senescence and vascular aging [1].

In triple-negative breast cancer cells, Nup93 depletion impairs cell invasion, migration, and proliferation by modulating genes related to actin cytoskeleton remodeling and epithelial-to-mesenchymal transition [3].

In cardiomyocytes, knockdown of Nup93 aggravates hypoxia-induced injury and cell death through abnormal regulation of gene transcription, mainly involving oxidative phosphorylation and ribosome subunits [4].

In summary, Nup93 is essential for maintaining normal cellular functions, especially in endothelial cell health, cell proliferation, and gene transcription regulation. Its dysfunction is associated with various diseases, including vascular aging, breast cancer, and heart failure. Studies using knockout models have significantly contributed to understanding these disease-related mechanisms, providing potential targets for therapeutic interventions [1,3,4].