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Owen et al. used single-cell RNA sequencing and spatial transcriptomics to analyze graft cells in heart transplants with cardiac allograft vasculopathy, showing that vascular smooth muscle cells and macrophages drive interferon-mediated inflammation and that JAK signaling blockade prolongs allograft survival.
Hu et al. show that the transmembrane glycoprotein CD98hc in cerebral endothelial cells regulates the integrin–FAK signaling pathway, thereby promoting angiogenesis and maintaining blood–brain barrier integrity.
Pathogenic variants in RBM20 cause an aggressive form of heart disease. van den Hoogenhof et al. show that overactivated CAMK2D drives this disease, and that pharmacological CAMK2D inhibition is a promising therapeutic approach in patients with RBM20 cardiomyopathy.
Momin et al. develop an antibody–siRNA conjugate to inhibit the secretion of osteopontin by the TREM2+ macrophages that expand during human atrial fibrillation. In mice, this approach reduced fibrosis and atrial fibrillation vulnerability.
Lu et al. report that PCBP1 safeguards AARS2 alternative splicing in the heart, and that loss of PCBP1 disrupts AARS2 splicing, leading to infantile mitochondrial cardiomyopathy. Loss of cardiac PCBP1 or AARS2 impairs oxidative phosphorylation and activates mitonuclear signaling and the unfolded protein response pathway.
Barone et al. identify a fetal-restricted wave of hematopoietic progenitors that emerge from the hemogenic endothelium before hematopoietic stem cells and substantially contribute to embryonic lympho-myelopoiesis.
Zhang et al. demonstrate that cardiac ischemia–reperfusion injury leads to the accumulation of glutamylated microtubules, which disrupts connexin 43 trafficking and promotes arrhythmias. They further show that targeting microtubule glutamylation or spastin preserves electrical stability and protects the heart from injury.
Wu et al. identify circulating proteins associated with cardiovascular and neurological imaging traits and diseases, and validate GDF15 as a shared determinant of heart and brain pathologies in mice.
Barrios et al. develop a multiview deep neural network to jointly analyze multiple echocardiographic video views, improving detection of cardiac anatomy and function.
Smyth et al. demonstrate that a cellular inhibitor of apoptosis, cIAP2, exacerbates inflammation and cardiac injury after myocardial infarction and that its inhibition, either genetically or via Smac mimetics, offers a promising immunotherapeutic strategy to reduce post-MI damage and progression to heart failure.
Li, Turaga and colleagues reveal intrinsic cardiomyocyte senescence and a hypoxic, mechanically stressed microvascular niche in hypoplastic left heart syndrome right ventricles and demonstrate that ventricular assist device therapy can alleviate these senescent states.
Kayman Kürekçi et al. show that fibulin-2 regulates epicardial cell activation through nuclear protein 1b signaling to balance fibrosis and regeneration after cardiac injury, and modulating this pathway can enhance heart regeneration in zebrafish.
Anderson et al. demonstrate that the glucokinase activator AZD1656 reduces inflammation and reverses cardiac dysfunction and metabolic remodeling in mice with diabetic cardiomyopathy.
Lazarevic et al. reveal a shared loss of a TBX5-dependent atrial gene network in cardiomyocytes and a disease-specific network gain in activated fibroblasts across atrial fibrillation and heart failure models.
Da Pra, Boriati and colleagues show that physiological glucocorticoids suppress growth-factor-induced cardiomyocyte regeneration by inhibiting ERK signaling and propose glucocorticoid receptor antagonism as a strategy to enhance their protective and regenerative effects.
Murphy et al. reveal a unifying pathogenetic mechanism according to which diverse mutations in the muscle-specific ribosomal protein RPL3L cause severe neonatal dilated cardiomyopathy, establishing a framework for interpreting the growing spectrum of RPL3L variants.
Saito et al. identify sphingosine kinase 1 as a critical regulator of physiological ductus arteriosus closure and pathological supravalvular aortic stenosis through its role in smooth muscle cell proliferation and propose potential therapeutics.
