Impact of Obesity on Microvascular Obstruction and Area at Risk in Patients After ST-Segment-Elevation Myocardial Infarction: A Magnetic Resonance Imaging Study.

Background: Better survival for overweight and obese patients after ST-segment elevation myocardial infarction (STEMI) has been demonstrated. The association between body mass index (BMI), microvascular obstruction (MVO), and area at risk (AAR) after STEMI was evaluated.

Methods: A prospective observational study was performed to enrolled patients undergoing primary percutaneous coronary intervention (pPCI) for STEMI and cardiac magnetic resonance was performed within 5-7 days.

Exosome-Mediated miR-155 Transfer from Smooth Muscle Cells to Endothelial Cells Induces Endothelial Injury and Promotes Atherosclerosis.

The vascular response to pro-atherosclerotic factors is a multifactorial process involving endothelial cells (ECs), macrophages (MACs), and smooth muscle cells (SMCs), although the mechanism by which these cell types communicate with each other in response to environmental cues is yet to be understood. Here, we show that miR-155, which is significantly expressed and secreted in Krüppel-like factor 5 (KLF5)-overexpressing vascular smooth muscle cells (VSMCs), is a potent regulator of endothelium barrier function through regulating endothelial targeting tight junction protein expression. VSMCs-derived exosomes mediate the transfer of KLF5-induced miR-155 from SMCs to ECs, which, in turn, destroys tight junctions and the integrity of endothelial barriers, leading to an increased endothelial permeability and enhanced atherosclerotic progression.

1, 25(OH)D-induced interaction of vitamin D receptor with p50 subunit of NF-κB suppresses the interaction between KLF5 and p50, contributing to inhibition of LPS-induced macrophage proliferation.

KLF5 and nuclear factor κB (NF-κB) regulate cell proliferation and inflammation. Vitamin D signaling through vitamin D receptor (VDR) exerts anti-proliferative and anti-inflammatory actions. However, an actual relationship between KLF5, NF-κB and VDR in the inflammation and proliferation of macrophages is still unclear.