Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Macrophage–fibroblast interactions have a central role in cardiac fibrosis. In response to left ventricular pressure overload, CCR2+ cardiac macrophages acquire a fibrogenic phenotype, secreting IL-1β and promoting the activation of a FAP+ POSTN+ fibroblast subpopulation through the transcription factor MEOX1. Macrophage-derived fibroblast-activating cytokines (such as IL-1β), growth factors and matricellular proteins contribute to the pathogenesis of heart failure.
Consumption of a high-fat diet leads to the progressive growth of atherosclerotic lesions. Two new studies document that, despite similar overall exposure to high-fat diet over a lifetime, an intermittent consumption of high-fat diet early in life accelerates atherosclerosis compared with continuous consumption of a high-fat diet. The mechanisms for accelerated atherosclerosis include reprogramming of macrophages and neutrophils.
In contrast to the ABYSS investigators’ interpretation of the primary results of their trial, we believe that β-blockers can be safely discontinued in the majority of patients after an uncomplicated myocardial infarction. However, in individuals developing symptoms of angina or heart failure, β-blocker treatment remains one of several guideline-recommended therapies.
A study using advanced single-cell technologies has broadened our understanding of the diversity and complexity of brain endothelial cells by uncovering new endothelial subtypes and transcriptional patterns. These findings offer insights into potential therapeutic targets and emphasize the need for further research on vascular lineages and neurovascular interactions.
