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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 3920195, 16 pages
Review Article

A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

1Department of Medical Surgical Sciences and Biotechnologies, “La Sapienza” University of Rome, Latina, Italy
2Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy
3Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
4Department of Medicine and Surgery, University of Salerno, 84081 Baronissi, Italy
5IRCCS, Bambino Gesù, Rome, Italy

Correspondence should be addressed to Giacomo Frati

Received 30 March 2017; Accepted 30 May 2017; Published 2 July 2017

Academic Editor: Stefano Toldo

Copyright © 2017 Leonardo Schirone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.