Daniel I. Simon

TL;DR: It is demonstrated that S-nitroso proteins form readily under physiologic conditions and possess EDRF-like effects of vasodilation and platelet inhibition, suggesting that S -nitrosothiol groups in proteins may serve as intermediates in the cellular metabolism of NO and raise the possibility of an additional type of cellular regulatory mechanism.

TL;DR: It is found that naturally produced nitric oxide circulates in plasma primarily complexed in S-nitrosothiol species, principal among which is S-Nitroso-serum albumin, which likely serves as a reservoir with which plasma levels of highly reactive, short-lived free nitrics can be regulated for the maintenance of vascular tone.

TL;DR: The presence of cathepsins K and S at sites of vascular matrix remodeling and the ability of SMC and macrophages to use these enzymes to degrade elastin supports a role for elastolytic cathePSins in vessel wall remodelling and identifies novel therapeutic targets in regulating plaque stability.

TL;DR: The studies implicate recruitment by KLF2 of the transcriptional coactivator cyclic AMP response element–binding protein (CBP/p300) as a unifying mechanism for these various effects of proinflammatory stimuli.

TL;DR: The platelet counterreceptor is identified as glycoprotein (GP) Ibα, a component of the GP Ib-IX-V complex, the platelet von Willebrand factor (vWf) receptor, which provides a molecular target for disrupting leukocyte–platelet complexes that promote vascular inflammation in thrombosis, atherosclerosis, and angioplasty-related restenosis.