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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.
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.
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 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.
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.
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.
Myocardial ischemia–reperfusion injury is more severe during the sleep-to-wake transition period of the day. A new study shows that timed administration of digoxin, a cardiac glycoside approved by the US Food and Drug Administration, prevents experimental myocardial ischemia–reperfusion injury by controlling proteostasis of the circadian-clock regulator Rev-Erbα.
Mutations in Kir2.1 resulting in defects in trafficking to the cardiomyocyte sarcolemma promote arrhythmia in Anderson–Tawil syndrome. Macias and colleagues provide a dual mechanism underlying cardiac arrhythmia that involves chaperoning of voltage-gated Na+ channels and a unique population of intracellular Kir2.1 channels that regulate Ca2+ cycling at the sarcoplasmic reticulum.
Late fetal liver hematopoiesis was thought to primarily rely on hematopoietic stem cells (HSCs). Using new genetic-tracing tools, a study shows that EVI1-positive HSCs mainly undergo expansion in the fetal liver, while differentiated blood cell production depends on HSC-independent intermediate hematopoietic progenitors.
A recent study by the GIGASTROKE consortium combines genetic discovery, fine-mapping and proteomic data to identify causal genes and variants related to disease. Results reveal known and new targets for prevention or treatment of stroke, and highlight the importance of genomics for drug discovery and development.
Changes in gene regulatory networks leading to species-specific variations in cardiac structure and function remain to be fully investigated. A new study presents a repertoire of human-gained (absent in mice) cis-regulatory elements, some of which appear to be involved in the acquisition of human-specific cardiac features.
Sex–age disparities in disease risk have been a neglected topic in cardiometabolic disease research. Zhernakova et al. demonstrate that risk factors and metabolic predictors covary with both sex and age: that is, men and women are different, and these differences are not static but change with age.
Recent developments in high-throughput, in-depth sequencing platforms are providing opportunities to improve our understanding of biology and disease. Here, Kuppe et al. use a combinatorial approach to relate transcriptional changes to translational and functional implications for the heart in response to myocardial infarction.
