Emerging Roles of Lysyl Oxidases in the Cardiovascular System

Lysyl oxidases (LOX and LOX-likes (LOXLs) isoenzymes) belong to a family of copper-dependent enzymes classically involved in the covalent cross-linking of collagen and elastin, a pivotal process that ensures extracellular matrix (ECM) stability and provides the tensile and elastic characteristics of...

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Detalles Bibliográficos
Autores: Martínez-González, José|||0000-0002-3894-7166, Varona, Saray|||0000-0002-7375-313X, Cañes Esteve, Laia|||0000-0002-9579-1321, Galán, María|||0000-0002-4758-8388, Briones, Ana|||0000-0001-8218-5579, Cachofeiro, Victoria, Rodríguez, Cristina|||0000-0002-6472-5647
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:253360
Acceso en línea:https://ddd.uab.cat/record/253360
https://dx.doi.org/urn:doi:10.3390/biom9100610
Access Level:acceso abierto
Palabra clave:Lysyl oxidases
Cardiovascular diseases
Atherosclerosis
Aortic aneurysm
Vascular calcification
Vascular stiffness
Myocardial fibrosis
Descripción
Sumario:Lysyl oxidases (LOX and LOX-likes (LOXLs) isoenzymes) belong to a family of copper-dependent enzymes classically involved in the covalent cross-linking of collagen and elastin, a pivotal process that ensures extracellular matrix (ECM) stability and provides the tensile and elastic characteristics of connective tissues. Besides this structural role, in the last years, novel biological properties have been attributed to these enzymes, which can critically influence cardiovascular function. LOX and LOXLs control cell proliferation, migration, adhesion, differentiation, oxidative stress, and transcriptional regulation and, thereby, their dysregulation has been linked to a myriad of cardiovascular pathologies. Lysyl oxidase could modulate virtually all stages of the atherosclerotic process, from endothelial dysfunction and plaque progression to calcification and rupture of advanced and complicated plaques, and contributes to vascular stiffness in hypertension. The alteration of LOX/LOXLs expression underlies the development of other vascular pathologies characterized by a destructive remodeling of the ECM, such as aneurysm and artery dissections, and contributes to the adverse myocardial remodeling and dysfunction in hypertension, myocardial infarction, and obesity. This review examines the most recent advances in the study of LOX and LOXLs biology and their pathophysiological role in cardiovascular diseases with special emphasis on their potential as therapeutic targets.