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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.
High-throughput sequencing technologies have revolutionized the study of transcription across cell types and many biological phenomena. Brash et al. have developed a resource based on 240 endothelial bulk RNA-sequencing datasets that uses machine learning to predict whether a gene is the product of leaky or active transcription.
Human pluripotent stem cells have been shown to be important models for interrogating the molecular basis for heart disease. This review highlights the contributions of these models to our understanding of inherited arrhythmia syndromes, with a focus on integrating mechanistic and genome-wide association study data.
Acute depletion of meningeal lymphatic vessels impairs the clearance of cerebrospinal fluid and brain macromolecules. A new study by Antila et al. shows that amyloid pathology in Alzheimer’s disease is neither improved nor aggravated by genetic expansion or depletion of meningeal lymphatic vessels.
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.
Hepatocytes are recognized as having a primary role in production and clearance of apolipoprotein B100-containing lipoproteins. A new study finds that Kupffer cells can respond to the initial atherogenic dyslipidemia and regulate levels of circulating lipoprotein.