Increasing autophagy and blocking Nrf2 suppress laminopathy-induced age-dependent cardiac dysfunction and shortened lifespan.

Mutations in the human LMNA gene cause a collection of diseases known as laminopathies. These include myocardial diseases that exhibit age-dependent penetrance of dysrhythmias and heart failure. The LMNA gene encodes A-type lamins, intermediate filaments that support nuclear structure and organize the genome.

Cementing Constrained Liners Into Secure Cementless Shells: A Minimum 15-Year Follow-Up Study.

Background: The authors and others have previously described the technique of cementing constrained liners into secure cementless acetabular shells and reported the short-term, average 3.9-year follow-up, using that technique. The purpose of the present study was to report the minimum 15-year follow-up of this same cohort.

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway.

Mutations in the human LMNA gene cause muscular dystrophy by mechanisms that are incompletely understood. The LMNA gene encodes A-type lamins, intermediate filaments that form a network underlying the inner nuclear membrane, providing structural support for the nucleus and organizing the genome. To better understand the pathogenesis caused by mutant lamins, we performed a structural and functional analysis on LMNA missense mutations identified in muscular dystrophy patients.