Limiting reductive stress for treating in-stent stenosis: the heart of the matter?
Restenosis after balloon angioplasty and stenting (BAS) remains an unsolved clinical dilemma for patients with coronary artery disease. A better understanding of the mechanisms that drive this phenomenon is likely to lead to more effective treatments. In this issue of the JCI, Ali et al. uncover a critical redox axis with the antioxidant enzyme glutathione peroxidase-1 (GPX1) at its hub and identify potential new therapeutic targets, such as ROS1 tyrosine kinase. This study represents a potential new approach to finding a treatment for BAS, with implications that may extend beyond BAS to other vasculopathies involving vascular remodeling.
Judy B
JB
de Haan
D000818:Animals; D050197:Atherosclerosis / Q000201:enzymology*; D005260:Female; D006801:Humans; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000201:enzymology*; D032389:Myocytes, Smooth Muscle / Q000201:enzymology*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D066253:Vascular Remodeling
D009124:Muscle Proteins; D011518:Proto-Oncogene Proteins; D011505:Protein-Tyrosine Kinases; C062333:ROS1 protein, human; D020794:Receptor Protein-Tyrosine Kinases; C483813:Ros1 protein, mouse