CircRNA circ-NNT mediates myocardial ischemia/reperfusion injury through activating pyroptosis by sponging miR-33a-5p and regulating USP46 expression.

Pyroptosis has been implicated in the pathophysiology of myocardial infarction (MI) in rodents, but its contribution to reperfusion injury in MI patients is unclear. Here, we evaluated pyroptosis in MI patients in vitro and in vivo models of myocardial ischemia/reperfusion (I/R) injury. We also investigated the molecular mechanisms that regulate pyroptosis and myocardial I/R injury in these in vitro and in vivo models.

Advanced Glycation End Products Enhance Murine Monocyte Proliferation in Bone Marrow and Prime Them into an Inflammatory Phenotype through MAPK Signaling.

Objective: Increased monocytes, particularly the inflammatory subset, are associated with accelerated atherosclerosis in diabetes through thus far incompletely defined mechanisms. The present study tested the hypothesis that advanced glycation end products (AGEs) promote bone marrow monocytes to proliferate and drive them into an inflammatory phenotype.

Methods And Results: In vivo, AGEs (25 mg/kg i.