Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins

ConclusionsAFM and molecular modeling were able to quantify distinct biomechanical and structural defects inLMNA mutations E161K, D192G, and N195K and correlate the defects with clinical phenotypic severity. Improvements in cellular biomechanical phenotype was demonstrated and may represent a mechanism of action for p38 MAPK inhibition therapy that is now being used in human clinical trials to treat laminopathies.
Source: Cardiovascular Research - Category: Cardiology Source Type: research