Drug repurposing to prevent pressure overload-induced cardiac hypertrophy and heart failure

This editorial refers to ‘Neuraminidase 1 is a driver of experimental cardiac hypertrophy’, by Q-Q. Chen et al., doi:10.1093/eurheartj/ehab347. The increase of cardiomyocyte size in response to pressure or volume overload encompasses an initial compensatory adaptive response to excessive haemodynamic or metabolic stress called cardiac hypertrophy.1,2 The persistence of this stress such as in cases of valve disease (e.g. aortic stenosis or regurgitation) or inadequately controlled arterial hypertension may lead to cardiac remodelling, ventricular dysfunction, and development of congestive heart failure, malignant arrhythmia, or sudden cardiac death.1,3 At the cellular level, the increased cardiomyocyte size is driven by increased protein synthesis and sequential addition of sarcomeres.1,2 These modifications are followed by changes in ion channels, extracellular matrix, and microvasculature.1,2 Since cardiomyocytes have little potential for cellular proliferation, many of the intracellular signalling pathways that regulate cell...