Nuclear pore complex aging

Nuclear pore complex (NPC) aging is the slow breakdown of the giant protein gates in your cell's nucleus over time. These pores (about 120 MDa each) perforate the nuclear envelope and control all traffic between the nucleus and the rest of the cell. The problem hits non-dividing cells hardest, like neurons, heart muscle, and skeletal muscle. Because they rarely divide, they cannot dilute old, damaged pores by making new cells. Some scaffold parts (nucleoporins like the Nup107-160 ring) last the cell's entire life without being replaced. As cells age, one inner-ring part (Nup93) picks up oxidative damage, especially carbonylation, while Nup107 stays unmodified (D'Angelo et al., Cell 2009). That damage makes the pore's selectivity filter, normally kept tight by floppy FG-repeat nucleoporins, progressively leaky. Cytoplasmic proteins like tubulin then slip into the nucleus, shown in aged rat neurons and in C. elegans. The result: the clean separation between nuclear jobs (transcription, DNA repair, RNA processing) and cytoplasmic ones breaks down, likely compounding other aging defects. In humans, NPC dysfunction is linked to age-related diseases like Alzheimer's and ALS/FTD, though cause-and-effect in living people is still unproven; most evidence is from rodents and invertebrates, and human data are largely associational.

Last reviewed: June 22, 2026

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