Guillermo García-Cardeña

TL;DR: This review traces the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explores its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerosis.

TL;DR: It is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells, indicating that the vascular endothelium is a target for leptin and suggesting a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.

TL;DR: Both short- and long-term exposure of human EC to VEGF stimulates the release of biologically active NO, suggesting that NO mediates aspects of V EGF signaling required for EC proliferation and organization in vitro.

TL;DR: Inhibition of signalling through Hsp90 attenuates both agonist-stimulated production of nitric oxide and endothelium-dependent relaxation of isolated blood vessels and indicates that in addition to its role as a molecular chaperone involved in protein folding and maturation, HSp90 may also be recruited to cellular targets depending on the activation state of the cell.

TL;DR: It is hypothesized that the selective and sustained expression of certain transcription factors and related “atheroprotective genes” in the endothelial lining of lesion‐protected areas represents a mechanism whereby hemodynamic forces can influence lesion formation and progression.