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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.
Eschenhagen and Weinberger provide a concise and comprehensive overview of the perspectives and challenges of heart repair with pluripotent stem cell-derived cardiomyocytes.
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.
By dissecting the cell composition and function of arterial grafts derived from the internal thoracic, radial and right gastroepiploic arteries, we identified factors that might promote patency rates of arterial grafts, including combating lipid deposition, disturbances in wall shear stress, smooth muscle cell proliferation, fibrosis and spasm.
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.
The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.
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.
The eye and the brain are both recognized as immune-privileged sites. Research now indicates that responses in the eye mirror those in the central nervous system (CNS), offering major implications for the treatment of CNS cancers and infections.
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.
On 21–23 September 2023, the Immuno-Cardiology Symposium was hosted by the Leducq Foundation Networks of Excellence Program (The Inflammatory-Fibrosis Axis in Adverse LV Remodeling: translating mechanisms into new diagnostics and therapeutics) at The Jackson Laboratory in Bar Harbor, Maine. The symposium highlighted recent advances in the basic science of dysregulated immune system activation and fibrosis in response to cardiac injury.
Adult hearts have inherently limited regenerative capabilities, such that injury results in lasting damage. The situation is different in neonatal mouse hearts, however, where a new study reveals a role for the immunomodulatory PD-1–PD-L1 pathway in regulating regeneration after injury.