Christine R Montague

TL;DR: In this article, the authors showed that extracellular matrix stiffening alone, which occurs during aging, can lead to endothelial monolayer disruption and atherosclerosis pathogenesis.

TL;DR: It is shown that matrix stiffness, separately from matrix density, can alter vascular growth and integrity, mimicking the changes that exist in tumor vasculature and suggest that therapeutically targeting tumor stiffness or the endothelial cell response to tumor stiffening may help restore vessel structure, minimize metastasis, and aid in drug delivery.

TL;DR: It is established that fatty acid and cholesterol assimilation are inexorably linked in Mtb and reveals a key function for Rv3723/LucA in in coordinating the transport of both these substrates.

TL;DR: It is discovered that Mtb is well adapted to use both lactate and pyruvate and that their metabolism requires gluconeogenesis, valine metabolism, the Krebs cycle, the GABA shunt, the glyoxylate shunt and the methylcitrate cycle.

TL;DR: Using in vitro and ex vivo models of vessel wall stiffness and aging, it is shown that stiffening of extracellular matrix within the intima promotes endothelial cell permeability—a hallmark of atherogenesis.