Cathepsin K-mediated notch1 activation contributes to neovascularization in response to hypoxia

Mitral valve endothelial cells secrete osteoprotegerin during endothelial mesenchymal transition

“…In addition, there is evidence that pharmacological cathepsin inhibition have a protective role in cardiovascular disease animal models[32]. Finally, cathepsin K (CatK) has been linked to endothelial cell invasion, proliferation and tube formation[33]. In this context, OPG and CatK have been described to be involved in vascular remodelling[34], leaving this intriguing possible association to be investigated in future studies addressing the MVP issue.…”

Renin inhibition reduces atherosclerotic plaque neovessel formation and regresses advanced atherosclerotic plaques

“…Angiogenic action stimulation has been closely linked to the Ang II/AT1R signaling pathway and protease activation (including matrix metalloproteinases (MMPs) and cysteinyl cathepsins) [8,11e13]. Cysteine protease cathepsins have also been implicated in the angiogenesis of pathophysiological conditions [14,15]. Several previous studies showed that cathepsin S (CatS) contributes to wound repair-or tumor growth-related angiogenesis [16,17].…”

Cathepsin K Deficiency Ameliorates Systemic Lupus Erythematosus-like Manifestations in Faslpr Mice

“…For example, normal human aortas or primary cultured vascular cells show negligible expression of CatK, but its expression greatly increases in vascular cells in atherosclerotic human lesions and abdominal aortic aneurysms (6–9). Besides its prominent roles in bone resorption, CatK also participates in the pathogenesis of many other diseases that do not associate with its activity in osteoclasts, including atherosclerosis (8, 10), lung fibrosis (11), obesity and diabetes (12, 13), abdominal aortic aneurysm (14), learning and memory deficits (15), and ischemia (16). …”