Proteases as clinical markers of adverse remodeling for heart failure in the aging population

Abstract

The heart failure (HF) burden, the aging population at large, and the aging population with HF have been increasing concurrently in developed countries worldwide. Epidemiological studies have warned that this trend will continue and lead to bankruptcy in health care unless new effective strategies and therapeutic targets are introduced. Translational studies have shown that adverse left ventricular (LV) remodeling is the principal mechanism for the march to HF after myocardial infarction (MI) and hypertension (HTN), the leading causes of HF in the elderly population aged>65 years. Evidence indicates that proteases play an important role in the remodeling that occurs at the extracellular as well as cellular, subcellular, and molecular levels and the march to HF. Besides the matrix metalloproteinases (MMPs) that play a critical role in extracellular matrix (ECM) and LV remodeling, several other proteases have also been implicated in adverse LV remodeling and dysfunction and the march to HF after MI, HTN, and cardiomyopathies. Several are released in the blood and can be imaged in the myocardium. Proteases are therefore attractive as potential clinical markers of adverse remodeling for HF in the aging population, not just for tools in diagnosis and follow-up but also in guiding therapy and prevention.