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.
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
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.
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.
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.