We hypothesized that repetitive hemolysis per se induces PH and angioproliferative vasculopathy and evaluated a new mechanism for hemolysis-associated PH (HA-PH) that involves the release of adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) from erythrocytes.
Loss-of-function mutations in CECR1 were associated with a spectrum of vascular and inflammatory phenotypes, ranging from early-onset recurrent stroke to systemic vasculopathy or vasculitis.
These are stimulators of interferon genes (STING)-associated vasculopathy of infancy (SAVI), which is a monogenic defect associated with excessive activity in interferon alpha and deficiency of adenosine deaminase 2, which is characterized by a polyarteritis nodosa-like picture.
ADAR1 levels and the extent of CTSS RNA editing are associated with changes in cathepsin S levels in patients with atherosclerotic vascular diseases, including subclinical atherosclerosis, coronary artery disease, aortic aneurysms and advanced carotid atherosclerotic disease.
These findings significantly augment our knowledge of BAI1 by showing a novel post-translational mechanism regulating BAI1 activity through cancer-associated proteases, have important implications for BAI1 function and regulation, and present novel opportunities for therapy of cancer and other vascular diseases.
These differences were detected despite the lack of by-phenotype differences in glycemic control, blood pressure level or presence of cardiovascular risk factor and suggest an active role of adiponectin in the pathophysiology of vascular disease in this population.
Here, we investigated the effect of adiponectin and TNFalpha on vascular calcification, a critical event in the development and progression of vascular disease.
Taken together, these data indicated that adiponectin promotes endothelial progenitor cell proliferation and migration via AMPK/Akt/eNOS signaling pathway and promotes tube formation through AMPK/eNOS, suggesting that adiponectin-transduced endothelial progenitor cell transplantation is a potential therapeutic target for vascular disease.
These results demonstrate that the AM-RAMP2 system exerts crucial vasoprotective effects after vascular injury and could be a therapeutic target for the treatment of vascular diseases.
Our results point to a complex interplay between the sex steroids and angiotensin-II in regulating adrenomedullin production by human endothelial cells, which may contribute to gender-related differences in vascular disease in humans.
The cell-to-cell interaction between monocytes and HUVECs induces AM production by HUVECs, which may play an important role in the pathogenesis of vascular disorders.