Lysyl oxidase and endothelial dysfunction: mechanisms of lysyl oxidase down-regulation by pro-inflammatory cytokines.

@article{Alcudia2008LysylOA,
  title={Lysyl oxidase and endothelial dysfunction: mechanisms of lysyl oxidase down-regulation by pro-inflammatory cytokines.},
  author={Javier F. Alcudia and Jos{\'e} Mart{\'i}nez-Gonz{\'a}lez and Anna Guadall and Mar{\'i}a Gonz{\'a}lez-D{\'i}ez and Lina Badim{\'o}n and Cristina Rodr{\'i}guez},
  journal={Frontiers in bioscience : a journal and virtual library},
  year={2008},
  volume={13},
  pages={
          2721-7
        }
}
Lysyl oxidase (LOX) plays a pivotal role in extracellular matrix (ECM) maturation. Furthermore, novel biological functions has been ascribed to LOX, among them cell differentiation, migration, transformation and regulation of gene expression. In this context, it has been suggested that abnormalities of LOX expression could underlie the development of multiple pathological processes including cardiovascular diseases. LOX seems to be crucial in the preservation of endothelial barrier function. In… 
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Lysyl Oxidase (LOX): Functional Contributions to Signaling Pathways
TLDR
Insight is provided into the diverse ways in which LOX participates in signaling events, and the mechanistic details and functional significance of the regulatory and cross-regulatory interactions of LOX with the EGFR, PDGF, VEGF, TGF-β, mechano-transduction, inflammatory and steroid signaling pathways are explored.
Statins normalize vascular lysyl oxidase down-regulation induced by proatherogenic risk factors.
TLDR
Modulation of LOX by statins could contribute to vascular protection and to the cardiovascular risk reduction achieved by this therapy, indicating that statins normalize vascular LOX expression altered by atherogenic risk factors through a RhoA/Rho kinase-dependent mechanism.
Hypoxia-induced ROS signaling is required for LOX up-regulation in endothelial cells.
TLDR
A role of Smad signaling and ROS in the up-regulation of LOX by hypoxia in endothelial cells is supported, which is independent of autocrine factors released by hypoxic cells and relies on a transcriptional mechanism.
TNF-α induced down-regulation of lysyl oxidase family in anterior cruciate ligament and medial collateral ligament fibroblasts.
The Role of the Lysyl Oxidases in Tissue Repair and Remodeling: A Concise Review
TLDR
The role of the LOXs in inflammation phase, proliferation phase, and tissue remodeling phase of the repair process is focused on to shed light on the understanding of its potential in tissue repair and provide up to date therapeutic strategies towards related injuries.
Lysyl oxidase inhibits TNF-α induced rat nucleus pulposus cell apoptosis via regulating Fas/FasL pathway and the p53 pathways.
The effect of BAPN on heart structure and function in the angiotensin II hypertensive mouse
TLDR
Results provide evidence that Angiotensin II-Induced hypertension causes the overexpression of LOX, and both the structural and mechanical changes can be extenuated with administration of the LOX suicide substrate BAPN.
Control of lung vascular permeability and endotoxin-induced pulmonary oedema by changes in extracellular matrix mechanics.
TLDR
The identification of lysyl oxidase and the extracellular matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability.
Screening of lysyl oxidase (LOX) and lysyl oxidase like (LOXL) enzyme expression and activity in preterm prelabor rupture of fetal membranes
TLDR
Increased LOX expression in pPROM, an OS-related disease, and the apparent inhibition of LOX activity by CSE restored by antioxidant treatment suggest that reactive oxygen species might influence LOX-mediated tissue remodeling in fetal membranes.
Lysyl oxidase activity in the ocular tissues and the role of LOX in proliferative diabetic retinopathy and rhegmatogenous retinal detachment.
TLDR
Lysyl oxidase activity showed a statistically significant decrease in the vitreous of PDR and RRD relative to control specimens, which can contribute to the inadequate collagen cross-linking that causes the ECM changes that occur in these diseases.
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