Gary H. Gibbons

TL;DR: Vascular remodeling is an active process of structural alteration that involves changes in at least four cellular processes -- cell growth, cell death, cell migration, and production or degradation of extracellular matrix -- and is dependent on a dynamic interaction between locally.

TL;DR: Direct evidence is provided that NO is an endogenous inhibitor of vascular lesion formation in vivo (by inhibiting smooth muscle cell proliferation and migration) and the possibility of ec-NOS transfection as a potential therapeutic approach to treat neointimal hyperplasia is suggested.

TL;DR: This study demonstrates that Ang II induces a severalfold increase in TGF beta 1 mRNA levels within 4 h that is dependent on de novo protein synthesis and appears to be mediated by activation of protein kinase C (PKC).

TL;DR: It is demonstrated that in these VSMC, TGF-beta 1 affects a key antiproliferative action, modulating the mitogenic properties of bFGF, a potent mitogen for VSMC.

TL;DR: It is demonstrated that significant sources of tissue ACE in human atherosclerotic plaques are regions of inflammatory cells, especially areas of clustered macrophages as well as microvessel endothelial cells, which suggest that ACE accumulation within the plaque may contribute to an increased production of local angiotensin that may participate in the pathobiology of coronary artery disease.