Shu Meng

TL;DR: The results indicate that ROS-driven Ca2+ signaling promotes vascular barrier dysfunction and that the SOCe machinery may provide crucial therapeutic targets to limit sepsis-induced ALI.

TL;DR: It is demonstrated for the first time that early hyperlipidemia promotes EC activation before monocyte recruitment via a caspase-1–sirtuin 1–activator protein-1 pathway, which provides an important insight into the development of novel therapeutics for blocking caspasing-1 activation as early intervention of metabolic cardiovascular diseases and inflammations.

TL;DR: It is suggested that IL-35 is an attractive novel therapeutic reagent for sepsis and cardiovascular diseases because it inhibits vascular response in acute inflammation and attenuates LPS-induced secretion of proinflammatory cytokines/chemokines.

TL;DR: It is demonstrated that HHcy and HG accelerated atherosclerosis and increased lesion monocytes and macrophages and further increased inflammatory MC and MØ levels in peripheral tissues and HHcy-lowering reversed circulating mononuclear cells, MC, and inflammatoryMC and MC-derived M Ø levels.

TL;DR: Hcy is a pro-inflammatory amino acid and induces inflammatory transcriptional signal pathways mediated by class 1 TFs, which are referred to as putative Hcy-responsive TFs.