it appears conceivable that a progerin-impaired nuclear envelope structure might allow nuclear leakiness, which could lead to phenotypical cell aging, including DNA damage and deficient response pathways (Musich and Zou, 2009). Most likely, nuclear malformations would also affect the envelope-embedded nuclear pore complex and its interaction partners, which are the main gatekeepers of compartmentalization (Capelson and Hetzer, 2009). Our results would thus favor a model where NCC becomes impaired in old cells as a consequence of altered gene expression and altered nuclear pore function (D’Angelo et al., 2009).
