MMP-2 and its implications on cardiac function and structure: Interplay with inflammation in hypertension.

Hypertension is one of the leading risk factors for the development of heart failure. Despite being a multifactorial disease, in recent years, preclinical and clinical studies suggest strong evidence of the pivotal role of inflammatory cells and cytokines in the remodeling process and cardiac dysfunction. During the heart remodeling, activation of extracellular matrix metalloproteinases (MMPs) occurs, with MMP-2 being one of the main proteases secreted by cardiomyocytes, fibroblasts, endothelial and inflammatory cells in cardiac tissue. In this review, we will address the process of cardiac remodeling and injury induced by the increase in MMP-2 and the main signaling pathways involving cytokines and inflammatory cells in the process of transcriptional, secretion and activation of MMP-2. In addition, an interaction and coordinated action between MMP-2 and inflammation are explored and significant in maintaining the cardiac cycle. These observations suggest that new therapeutic opportunities targeting MMP-2 could be used to reduce inflammatory biomarkers and reduce cardiac damage in hypertension.
Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Elen Rizzi reports financial support was provided by Fundacao de Amparo à Pesquisa do Estado de São Paulo (FAPESP). Elen Rizzi reports financial support was provided by Coordenacao de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). Elen Rizzi reports financial support and administrative support were provided by University of Ribeirao Preto (UNAERP). Stefany Bruno Cau reports financial support was provided by Fundacao de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG). Stefany Bruno Cau reports financial support, administrative support, and equipment, drugs, or supplies were provided by Federal University of Minas Gerais (UFMG). Alejandro Ferraz do Prado reports financial support was provided by Fundacao Amazônia de Amparo a Estudos e Pesquisas (FAPESPA). Thais Ribeiro Vitorino reports financial support was provided by Fundacao de Amparo à Pesquisa do Estado de São Paulo (FAPESP). Thais Ribeiro Vitorino reports financial support was provided by Coordenacao de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).
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