Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3030624 | Trends in Cardiovascular Medicine | 2010 | 5 Pages |
Abstract
Mutations in the lamin A/C gene (LMNA) encoding A-type nuclear lamins cause dilated cardiomyopathy. We have uncovered a novel connection between these mutations and hyperactivation of the extracellular signal-regulated kinase 1/2 and c-jun N-terminal kinase branches of the mitogen-activated protein kinase signaling pathway in a mouse model of the disease. This discovery has identified targets that can be inhibited by drugs that improve heart function and prevent fibrosis.
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Authors
Antoine Muchir, Wei Wu, Howard J. Worman,