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We report a new non-invasive approach to track neutrophils in both mice and humans by directing multimodal fluorine-loaded nanotracers equipped with specific binding peptides to neutrophil surface markers to enable background-free readout by in vivo 19F MRI.
Tissue infiltration of neutrophils is a key event of sterile and pathogen-induced inflammation; however, there is at present no non-invasive tool to visualize neutrophil dynamics in the body. Bouvain et al. develop a neutrophil-specific tracer that enables longitudinal imaging of neutrophil flux across the whole body.
Clonal hematopoiesis of indeterminate potential (CHIP) is a blood disorder that can increase the risk of cardiovascular disease. A new study reveals that CHIP driven by somatic mutations in DNA damage repair genes increases the risk of CVD in humans, and provides mechanistic insights in murine models.
Using cap analysis of gene expression, we have constructed a map of the genome regulatory network (promoters and enhancers) in healthy and failing human hearts. Analysis of this map demonstrates differential transcriptional regulation in cardiac chambers, disease states, and ischemic and non-ischemic cardiomyopathies. This information could lead to tailored therapies.
Wen Tan et al. review the current technologies available for single-cell transcriptomics, epigenomics and multi-omics analyses, their impact on the cardiovascular research and possible future applications.
Regulatory elements including promoters and enhancers control tissue- and context-dependent gene expression. A new study presents an atlas of transcribed regulatory elements in human heart compartments, and their changes in transcription in the failing heart.
Supplementation with the gut microbial-derived metabolites acetate and butyrate has been shown to lower blood pressure in experimental models of hypertension. However, the translational potential of these metabolites has been unexplored. We provide clinical evidence that acetate and butyrate lower blood pressure in untreated patients with hypertension.
Increasing evidence suggests that IGFBP7 may be an accurate biomarker for heart failure. A new study shows that beyond its diagnostic value, IGFBP7 may drive the detrimental effects of pressure overload in mice by a mechanism that, at least in part, involves the regulation of senescence by an IGF-1R–IR–FOXO3a signaling cascade.
The epicardium has an active role in the formation of fetal and neonatal mammalian hearts, which retain the ability to regenerate. A single-cell comparison of human fetal and adult epicardial cells defines the transcriptomic programs that are specific to the fetal epicardium that could be harnessed to repair the injured adult heart.
Pioneering cohort studies including the Framingham Heart Study have led to major insights into cardiovascular disease. However, these studies are underpowered to identify the effects of less common risk factors on human health. This has motivated the development of the UK Biobank, a biomedical database linking health and genetic information in 500,000 individuals.
Endothelial cell–cell contacts in blood vessels constitute a barrier to the flux of molecules and cells from blood to tissues. We identified the tyrosine-protein kinase Yes as the principal regulator of collective endothelial cell migration and vascular barrier dynamics, a finding that opens avenues for future therapeutic development.
Postural orthostatic tachycardia syndrome (POTS) has been observed following SARS-CoV-2 infection. In this study, we observed occurences of POTS following COVID-19 vaccination, albeit at a lower rate than following COVID-19 infection.
Postural orthostatic tachycardia syndrome (POTS) can follow COVID-19 as part of the post-acute sequelae of SARS-CoV-2 infection, but it can also develop after COVID-19 vaccination, although at a lower frequency.
The contribution of platelets to atherothrombosis is well established. Accumulating genome-wide association studies have revealed several variants of genes encoding molecules along the nitric oxide (NO)–soluble guanylyl cyclase (sGC)–cyclic guanosine-3′,5′-monophosphate (cGMP) pathway that are associated with increased risk of coronary artery disease; however, the cell types and functional impact of these risk variants remain poorly understood. Mauersberger et al. now demonstrate that platelet-specific knockout of a transcript encoding sGC increased atherosclerosis, whereas pharmacological stimulators of sGC reduced lesions via a paracrine effect of angiopoietin-1 on endothelial cell–leukocyte interactions.
Clustering the atherosclerotic plaques of patients based on gene expression unearths novel and clinically relevant heterogeneity beyond the established dogma of ‘stable’ and ‘unstable’ plaques.
Preemptive identification of unstable, ‘vulnerable’ atherosclerotic plaques is important for predicting the risk of thrombotic events. A new study shows that unbiased classification of human atherosclerotic plaques on the basis of transcriptomic features identifies subgroups with distinct biology and clinical presentation.
Regulation of endothelial barrier function is critical to physiological function of the vasculature, which must dynamically change in many physiologic and pathologic settings. A new study emphasizes the complex relationship between VE-cadherin phosphorylation and vascular leak and the critical role of the tyrosine kinase Yes in this process.
A new study shows that brain-resident parenchymal border macrophages (PBMs) maintain perivascular extracellular matrix composition by the release of matrix metalloproteinases. Depletion of PBMs suppressed glymphatic fluid transport, underscoring their responsibility for perivascular space homeostasis and brain protein clearance.
Cytotoxic T cells react to cardiac peptides in patients with cancer that receive immunotherapy, resulting in myocarditis. Identifying the targets for T cells in patients who are immunosuppressed will enable a better understanding of individual risk before treatment is initiated
The mechanisms of adrenergic stimulation of cardiac voltage-gated calcium (CaV) channels have remained elusive. Using proximity proteomics and genetically altered mice, we show that phosphorylation of the CaV channel inhibitor Rad is essential for regulation, by the sympathetic nervous system, of calcium influx, and for augmentation of cardiac contractility.
