We compared the plasma CTSS as well as other biomarkers of atherosclerosis in patients with abdominal aortic aneurysms (AAA) and aortoiliac occlusive disease (AOD), aiming to identify the underlying pathogenic mechanisms of the disease development.
Consistent with the loss of H<sub>2</sub>S, human antigen R sulfhydration was attenuated in atherosclerosis and resulted in the stabilization of human antigen R-target mRNAs, for example, CD62E and cathepsin S, both of which are linked to endothelial cell activation and atherosclerosis.
Conclusions These results demonstrate an essential role of CatS in chronic stress-related neointimal hyperplasia in response to injury, possibly via the reduction of toll-like receptor-2/toll-like receptor-4-mediated inflammation, immune action, and smooth muscle cell proliferation, suggesting that CatS will be a novel therapeutic target for stress-related atherosclerosis-based cardiovascular disease.
Here we show that cathepsin S mRNA (CTSS), which encodes a cysteine protease associated with angiogenesis and atherosclerosis, is highly edited in human endothelial cells.
CTSS mRNA levels correlated with CD40 mRNA levels, independently of observed traditional risk factors for atherosclerosis and pharmacological treatment.
Since this enzyme has been implicated in the development of atherosclerotic lesions, we propose that cathepsin S represents a molecular link between obesity and atherosclerosis.
Because of the importance of the CTSS gene product in vascular matrix remodeling, this polymorphism may be useful in the study of associations with atherosclerosis and related phenotypes.