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Malik, Beaufort et al. show that rare and common genetic variations in HTRA1 associate with stroke and coronary artery disease outcomes via independent mechanisms.
Rasheed et al. show that dysregulation of lipid metabolism uniquely affects splenic endothelial cells of the hematopoietic niche, which promotes extramedullary myelopoiesis and contributes to plaque accumulation during atherosclerosis.
Elevated Lp(a) is an independent atherosclerosis risk factor that is not routinely measured in the general population. Aminorroaya et al. develop and validate a machine learning model, ARISE, that allows for the detection of elevated Lp(a) using commonly available clinical features from electronic records.
Hamidzada et al. show that human pluripotent stem cell–derived macrophages are educated into a tissue-resident fate within human cardiac microtissues, enhancing its function via efferocytic ingestion of stressed cardiomyocyte cargo.
Based on comparative single-cell transcriptomics of arterial grafts deriving from internal thoracic, radial and right gastroepiploic arteries, Hu, Dai, Chang, et al. identify factors that might prevent extracellular matrix deposition and fibrosis and improve the outcomes of coronary artery bypass grafting.
Tuz et al. report that stroke and myocardial infarction induce the release of neutrophil extracellular traps (NETs), triggering the loss of B cells and a decrease in immunoglobulin A secretion, and that inhibition of NETs prevents the loss of immunoglobulin A in mice and in patients with stroke.
In a retrospective cohort study examining the comparative effectiveness of diabetes drugs in adults at moderate risk for cardiovascular disease, GLP-1 receptor agonists and SGLT2 inhibitors reduced the risk of cardiovascular events compared to DPP4 inhibitors, whereas sulfonylureas increased the risk.
Antila et al. show that brain amyloid-β load is not significantly affected by sustained dural lymphatic vessel atrophy or hyperplasia induced by lymphangiogenic growth factor manipulation in two mouse models of Alzheimer’s disease.
Brash et al. created the BulkECexplorer, an online tool based on 240 endothelial bulk RNA-seq datasets, which predicts active or leaky gene expression in five vascular endothelial cell subtypes.
Piollet, Porsch et al. report that the myeloid receptor TREM2 limits necrotic core formation in atherosclerosis and controls key atherosclerosis-related functions of macrophages, such as efferocytosis, lipid uptake and foam cell survival.
Using two complementary approaches to induce hypercholesterolemia in mice, Di Nunzio, Hellberg, Zhang, Ahmed et al. identified liver macrophages as key cells that organize the systemic responses to lipoproteins during the initial phases of atherosclerosis pathogenesis.
Ahmed, Nguyen et al. show that two FDA-approved antibiotics, paromomycin and neomycin, promote cardiomyocyte proliferation and improve cardiac function after myocardial infarction in mice and pigs by interfering with the cell division inhibiting function of transcription factors Meis1 and Hoxb13.
Horitani, Chavkin et al. report that the loss of the Y chromosome in macrophages from failing human hearts correlates with cardiac fibroblast activation and that the deficiency of a single Y chromosome gene, Uty, triggers an epigenetic rewiring in macrophages toward a profibrotic phenotype and increases cardiac fibrosis and dysfunction that can be prevented by TGFβ-neutralizing antibodies.
Vargas Aguilar et al. report that the PD-1–PD-L1 checkpoint-inhibitor pathway is highly active in heart-resident and circulating immune cells of newborn mice and disruption of this pathway led to increased inflammation and pathogenic T cell activity, impairing regeneration.
A multistate analysis of 341,159 adults from the UK Biobank shows that the development and mortality of cardiometabolic multimorbidity are associated with biological aging, as measured by the Klemera–Doubal Method Biological Age and PhenoAge algorithms.
By performing a genome-wide CRISPR screen in human induced pluripotent stem cells, Padmanabhan et al. identify the acetyl-lysine reader protein BRD4 as a regulator of cardiomyocyte differentiation, and they validate in vivo that BRD4 is required during development for the fate determination of a subset of secondary heart field cardiac progenitor cells.
Perez-Shibayama et al. report that BMP4 signaling is downregulated in autoimmune myocarditis. Restoring BMP4 levels with antibodies that neutralize the BMP inhibitors gremlin-1 and gremlin-2 can ameliorate cardiac inflammation and improve function in mouse models.
Using single-cell RNA sequencing, spatial transcriptomics and genetic experiments, Li et al. report that the close interaction of a specific cardiomyocyte subtype (aCM2), fibroblasts expressing the complement C3 and macrophages expressing C3ar1 was observed in pro-renewal conditions, such as regenerative neonatal hearts and hearts of adult mice overexpressing an active form of YAP in cardiomyocytes.
Gustafsson, Lampa et al. used proteomics, metabolomics and clinical factors in a case–cohort study to identify biomarkers of imminent myocardial infarction and devise a prediction model for imminent myocardial infarction, which can be clinically used in the general population.