Emerging roles of lysyl oxidases in the cardiovascular system: New concepts and therapeutic challenges
Entity
UAM. Departamento de Farmacología; Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)Publisher
MDPI, Basel, SwitzerlandDate
2019-10-14Citation
10.3390/biom9100610
Biomolecules 9.10 (2019): 610
ISSN
2218-273XDOI
10.3390/biom9100610Funded by
The authors thank the support provided by the Spanish Ministerio de Ciencia, Innovación y Universidades (MICIU), Instituto de Salud Carlos III (ISCIII) [grants RTI2018-094727-B-100, PI18/0919,] and Agencia de Gestio d’Ajuts Universitaris i de Recerca (AGAUR; program of Support to Research Groups, Ref. 2017-SGR-00333). Our studies were also co-founded by Fondo Europeo de Desarrollo Regional (FEDER), a way to make Europe. L.C. and M.G. were supported by a FI fellowship (AGAUR) and the Miguel de Servet Program (ISCIII; CP15/00126) respectivelyProject
Gobierno de España. RTI2018-094727-B-100; Gobierno de España. PI18/0919Editor's Version
https://doi.org/10.3390/biom9100610Subjects
Lsyl oxidases; Cardiovascular diseases; Atherosclerosis; Aortic aneurysm; Vascular calcificationen; Vascular stiffness; Myocardial fibrosis; FarmaciaRights
© 2019 by the authors. Licensee MDPI, Basel, SwitzerlandAbstract
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, di erentiation, 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 sti ness 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
Files in this item
Google Scholar:Martínez-González, José
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Varona, Saray
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Cañes, Laia
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Galán, María
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Briones Alonso, Ana María
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Cachofeiro, Victoria
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Rodríguez, Cristina
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