Human lysyl oxidase over-expression enhances baseline cardiac oxidative stress but does not aggravate ros generation or infarct size following myocardial ischemia-reperfusion
Valls-Lacalle, Laura (Instituto de Salud Carlos III)
Puertas Umbert, Lídia (Institut d'Investigació Biomèdica Sant Pau)
Varona, Saray (Institut d'Investigació Biomèdica Sant Pau)
Martínez-González, José (Institut d'Investigació Biomèdica Sant Pau)
Rodríguez, Cristina (Institut d'Investigació Biomèdica Sant Pau)
Rodríguez-Sinovas, Antonio (Instituto de Salud Carlos III)
Universitat Autònoma de Barcelona

Date:	2022
Abstract:	Lysyl oxidase (LOX) is an enzyme critically involved in collagen maturation, whose activity releases HO as a by-product. Previous studies demonstrated that LOX over-expression enhances reactive oxygen species (ROS) production and exacerbates cardiac remodeling induced by pressure overload. However, whether LOX influences acute myocardial infarction and post-infarct left ventricular remodeling and the contribution of LOX to myocardial oxidative stress following ischemia-reperfusion have not been analyzed. Isolated hearts from transgenic mice over-expressing human LOX in the heart (TgLOX) and wild-type (WT) littermates were subjected to global ischemia and reperfusion. Although under basal conditions LOX transgenesis is associated with higher cardiac superoxide levels than WT mice, no differences in ROS production were detected in ischemic hearts and a comparable acute ischemia-reperfusion injury was observed (infarct size: 56. 24 ± 9. 44 vs. 48. 63 ± 2. 99% of cardiac weight in WT and TgLOX, respectively). Further, similar changes in cardiac dimensions and function were observed in TgLOX and WT mice 28 days after myocardial infarction induced by transient left anterior descending (LAD) coronary artery occlusion, and no differences in scar area were detected (20. 29 ± 3. 10 vs. 21. 83 ± 2. 83% of left ventricle). Our data evidence that, although LOX transgenesis induces baseline myocardial oxidative stress, neither ROS production, infarct size, nor post-infarction cardiac remodeling were exacerbated following myocardial ischemia-reperfusion.
Grants:	Instituto de Salud Carlos III PI17/01397
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	Cardiac remodeling ; Lysyl oxidase ; Reperfusion injury
Published in:	Antioxidants, Vol. 11 Núm. 1 (january 2022) , p. 75, ISSN 2076-3921

DOI: 10.3390/antiox11010075
PMID: 35052579

15 p, 2.7 MB

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Research literature > UAB research groups literature > Research Centres and Groups (research output) > Health sciences and biosciences > Institut de Recerca Sant Pau
Articles > Research articles
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