Abstract
Cardiac remodeling is induced by a multitude of stimuli, including myocardial infarction, pressure and/or volume overload, and genetics; and involves matrix metalloproteinases (MMPs) every step of the way [1]. While cardiac remodeling is initially a compensatory response, the transition to adverse remodeling frequently culminates in the development of congestive heart failure (CHF), and CHF is a significant contributor to cardiovascular morbidity and mortality rates. This chapter will define cardiac remodeling, describe MMP-dependent mechanisms that stimulate the remodeling process, and explore future directions and therapeutic potentials in terms of MMP inhibition. We will focus on the primary diseases that stimulate cardiac remodeling in humans, namely myocardial infarction and hypertension. Understanding how cardiac remodeling evolves from an initially beneficial mechanism to a maladaptive event and how MMPs influence these stages will potentially provide us with markers to predict adverse events in the clinic.
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Lin, J., Lindsey, M.L. (2008). MMP roles in the initiation and progression of cardiac remodeling leading to congestive heart failure. In: Lagente, V., Boichot, E. (eds) Matrix Metalloproteinases in Tissue Remodelling and Inflammation. Progress in Inflammation Research. Birkhäuser Basel. https://doi.org/10.1007/978-3-7643-8585-9_7
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DOI: https://doi.org/10.1007/978-3-7643-8585-9_7
Publisher Name: Birkhäuser Basel
Print ISBN: 978-3-7643-8584-2
Online ISBN: 978-3-7643-8585-9
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