Limiting reductive stress for treating in-stent stenosis: the heart of the matter?
Level V
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- Record sourced from PubMed, PMID 25401464.
- Also identified by DOI 10.1172/JCI79423 and PMC identifier 4348949.
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Abstract
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.
Medical subject headings
- Atherosclerosis
- Muscle Proteins
- Muscle, Smooth, Vascular
- Myocytes, Smooth Muscle
- Protein-Tyrosine Kinases
- Proto-Oncogene Proteins
- Receptor Protein-Tyrosine Kinases
- Vascular Remodeling