Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins

Given the clinical impact of LMNA cardiomyopathies, understanding lamin function will fulfill a clinical need and will lead to advancement in the treatment of heart failure. A multidisciplinary approach combining cell biology, atomic force microscopy (AFM) and molecular modeling was used to analyze the biomechanical properties of human lamin A/C gene (LMNA) mutations (E161K, D192G, N195K) using an in vitro neonatal rat ventricular myocyte (NRVM) model.



Titolo: Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins
Autori: 
LAURINI, ERIK
MARTINELLI, VALENTINA
LANZICHER, THOMAS
PUZZI, LUCA
BORIN, DANIELE
MESTRONI, LUISA
SBAIZERO, ORFEO (Corresponding)
PRICL, SABRINA
mostra contributor esterni 
Data di pubblicazione: 2018
Data ahead of print: 8-feb-2018
Stato di pubblicazione: Pubblicato
Rivista: 
CARDIOVASCULAR RESEARCH  
Abstract: Given the clinical impact of LMNA cardiomyopathies, understanding lamin function will fulfill a clinical need and will lead to advancement in the treatment of heart failure. A multidisciplinary approach combining cell biology, atomic force microscopy (AFM) and molecular modeling was used to analyze the biomechanical properties of human lamin A/C gene (LMNA) mutations (E161K, D192G, N195K) using an in vitro neonatal rat ventricular myocyte (NRVM) model.
Handle: http://hdl.handle.net/11368/2917991
Digital Object Identifier (DOI): http://dx.doi.org/10.1093/cvr/cvy040
URL: https://academic.oup.com/cardiovascres/advance-article/doi/10.1093/cvr/cvy040/4844873
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