English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Heart disease is a major cause of morbidity and premature mortality. Cardiomyopathy is an anatomic and pathologic condition associated with muscle and electrical dysfunction of the heart, often leading to heart failure–related disability. Dilated cardiomyopathy caused by mutations in A-type lamin gene (i.e., LMNA cardiomyopathy) is characterized by an increase in both myocardial mass and volume. The ventricular walls become thin and stretched, compromising cardiac contractility and ultimately resulting in poor left ventricular function. Despite current strategies to aggressively manage “LMNA cardiomyopathy,” the disorder remains a common cause of heart failure with decreased ejection fraction, and a prevalent diagnosis in individuals is referred for cardiac transplantation. Despite progress in reducing “LMNA cardiomyopathy”–relatedmortality, hospitalizations remain very frequent and rates of readmission continue to rise. It appears important and necessary to further increase our knowledge on the pathophysiology of “LMNA cardiomyopathy” to unveil novel molecular/cellular mechanisms to target future therapeutic approaches.

Cardiomyopathy Caused by Mutations in Nuclear A-Type Lamin Gene