Lamins as mediators of oxidative stress

The nuclear lamina defines both structural and functional properties of the eukaryotic cell nucleus. Mutations in the LMNA gene, encoding A-type lamins, lead to a broad spectrum of diseases termed laminopathies. While different hypotheses have been postulated to explain disease development, there is still no unified view on the mechanistic basis of laminopathies. Recent observations indicate that laminopathies are often accompanied by altered levels of reactive oxygen species and a higher susceptibility to oxidative stress at the cellular level. In this review, we highlight the role of reactive oxygen species for cell function and disease development in the context of laminopathies and present a framework of non-exclusive mechanisms to explain the reciprocal interactions between a dysfunctional lamina and altered redox homeostasis.

► The nuclear lamina defines structural and functional properties of the cell nucleus.
► Lamina dysfunction leads to a broad spectrum of laminopathies.
► Recent data is reviewed connecting laminopathies to oxidative stress.
► A framework is proposed to explain interactions between lamins and oxidative stress.