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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.
The border zone in myocardial infarction is of key importance for the remodeling process that drives heart failure and sudden cardiac death. Two studies have now performed single-nucleus and spatial mapping of mouse myocardial infarction to provide novel insights into spatiotemporal events in the border zone.
Loss of VEGF-C or VEGFR3 function or gain of VE-cadherin function causes identical defects in sinusoidal and lymphatic growth, resulting in anemia and lymphedema. Mechanistically, VEGF-C drives VE-cadherin phosphorylation and endocytosis whereas VE-cadherin prevents VEGFR3 internalization and downstream growth factor signaling. In the absence of VEGFR3, reducing VE-cadherin levels rescues vascular growth by potentiating VEGF-C–VEGFR2 signaling.
GPR55 is a G protein–coupled receptor that is activated by endogenous lipid mediators. Our findings in experimental mouse models of atherosclerosis and human plaques indicate that GRP55 signaling is important for limiting B cell activation and humoral responses during hypercholesterolemia, which suggests that GPR55 signaling has an atheroprotective role.
The rapid enhancement of cardiac Ca2+ current (ICa,L) is central to enhanced heart function during the sympathetic fight-or-flight response. A new study shows how the small GTPase Rad mediates tonic ICa,L inhibition that is relieved after PKA-dependent phosphorylation of Rad, which causes release of Rad from the Ca2+ channel and increased ICa,L.
Myocardial ischemia–reperfusion injury (MIRI) substantially contributes to the morbidity associated with ischemic heart disease. Timed administration of digoxin decreased the susceptibility of mouse cardiomyocytes to MIRI; digoxin acted by promoting proteasomal degradation of the nuclear receptor REV-ERBα, a key component of the molecular circadian clock.
Sinusoidal vessels are specialized vascular structures required for hematopoiesis. A new study demonstrates a role for VEGF-C–VEGFR3 signaling in the development of sinusoidal vessels and a previously unappreciated reciprocal regulatory relationship between VE-cadherin and VEGFR3.
B cells have an essential role in regulating atherogenesis. A new study shows that the orphan receptor GPR55 is a pivotal modulator of B cell maturation and immunoglobulin production. This new finding identifies a previously uncharacterized protein involved in regulation of atherosclerosis by the immune system.
