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Structural determination of the ABCC4 transporter is a major first step in providing crucial molecular insights into the transport of platelet substrates into granules, as well as drug transport from platelets. The findings provide a framework for understanding platelet interactions and potential design of specific platelet antagonists.
Vascular patterning is dictated by transcription factors, such as the Notch pathway. Molecular profiling has uncovered snapshots of the transcriptional specification of endothelial cell tubulogenesis. Here, the authors leverage the output of Notch signaling, demonstrating that vascular remodeling is poorly predicted by transcriptional profiling.
Ranolazine is an anti-arrhythmic drug that targets voltage-gated sodium channels. Lenaeus et al. present a cryo-EM structure of the cardiac sodium channel bound to ranolazine to demonstrate that this compound acts as a structural clamp that inhibits the channels.
The plasma of individuals with atherosclerosis contains cytokines that induce a pathogenic signaling cascade in immune cells. Saracatinib, a dual kinase inhibitor that targets the tyrosine kinases SRC and BCR-ABL, can prevent activation of this phospho-signaling pathway implicated in the pathogenesis of cardiovascular disease.
Statins exert cardiovascular protective effects that are independent of cholesterol lowering. Using endothelial cells derived from induced pluripotent stem cells, Liu et al. show that statins can improve endothelial dysfunction by inhibiting endothelial–mesenchymal transition via epigenetic regulation of the GGTase–RhoA–YAP1–SOX9 signaling pathway.
Preserving hemostasis while preventing pathological thrombosis has been a central goal in drug development. A new way to restore hemostasis is suggested by the finding that glycoprotein V is cleaved by thrombin on activated platelets, negatively regulating clotting at sites of vascular injury.
Calcium sparks are the elementary detectable units of calcium release through ryanodine receptors (RyRs). Hou et al. correlate Ca2+ sparks with RyR cluster configurations and provide insights into the dynamics of Ca2+ release in live cardiomyocytes at baseline and in pathological conditions.
Specialized endothelial cells within certain embryonic blood vessels can generate hematopoietic cells. A recent study reveals blood-forming capacity also within embryonic lymphatic endothelium, which is suppressed during normal development by the lymphatic endothelial fate-determining transcription factor PROX1.
A body of experimental studies has pointed to a role for autoimmunity in atherosclerosis in animal models. Translational studies using single-cell sequencing now confirm that is also true of the atherosclerotic plaque development in humans.
The mechanisms that link altered metabolism and heart failure remain unclear. A new study defines the role of the lysine demethylase KDM8 in preventing the initiation of dilated cardiomyopathy through epigenetic control of homeostatic cardiac metabolism.
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.
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.
