ATVB Featured Articles June 2020

Published: May 28, 2020

ATVB Journal cover

About the Cover

A macrophage in coculture with aortic valve interstitial cells. The coculture was stained with DAPI (blue, nuclei), phalloidin (yellow, F-actin), and by immunofluorescence with anti-CD68 antibody (pink) to identify macrophages. (See pages e153–e165.)

Macrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing

Announcement from our Editor-in-Chief, Dr. Alan Daugherty

ATVB is pleased to announce that we are now considering Research Letters for publication. Please visit https://www.ahajournals.org/atvb/article-types for additional information.


Editor's Pick

Galectin-3 may serve as a novel marker for a protective macrophage subset during atherosclerosis progression. Whereas, MMP-12 can cleave galectin-3 and drive pro-inflammatory macrophage polarization.

Galectin-3 identifies a subset of macrophages with a potential beneficial role in atherosclerosis
K Di Gregoli, M Somerville, R Bianco, AC Thomas, A Frankow, AC Newby, SJ George, CL Jackson and JL Johnson

Editor's Note:
This article reports that galectin-3 deficiency in apolipoprotein E -/- mice leads to altered plaque composition. This article also highlights a new mechanism where MMP12-dependent cleavage of galectin-3 promotes pro-inflammatory macrophage polarization.


Featured Articles

Anti-platelet effects of clopidogrel may be impaired in the setting of diabetes due to reduced hepatic pro-drug bioactivation, which is mediated by interleukin-1 receptor signaling.

Clopidogrel resistance in a murine model of diet-induced obesity is mediated by the interleukin-1 receptor and overcome with DT-678

Related Editorial: IL-1R (Interleukin-1 Receptor) Signaling and Attenuated Hepatic CYP (Cytochrome P450) 2C Expression: Explanation for Higher Rate of Clopidogrel Resistance in Patients With Diabetes Mellitus?
 

 

Dysregulated EP4 overexpression in vascular smooth muscle cells promotes inflammatory monocyte/macrophage infiltration and attenuates elastin/collagen fiber formation, leading to AAA exacerbation.

Excessive EP4 signaling in smooth muscle cells induces abdominal aortic aneurysm by amplifying inflammation