Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Elezaby et al. show that cardiac troponin I interacts with mitochondrial ATP synthase to increase ATPase activity. Disrupting this interaction reduces cardiac damage following transient ischemia.
Bayer et al. show that CD8+ T cells contribute to the adverse cardiac effect of doxorubicin administration, promoting fibroblast activation and inflammation through a mechanism dependent on IFNγ and the degranulation of granzyme B.
Haykin et al. show that activation of the brain’s reward system modulates adrenergic input to the liver and complement component 3 transcription, affecting vascularization and improving cardiac recovery after acute myocardial infarction.
Prabhakar et al. demonstrate in rats with mitomycin C-caused pulmonary veno-occlusive disease activation of protein kinase R (PKR) and the integrated stress response (ISR), leading to the depletion of VE-cadherin and RAD51 from endothelial junctions, endothelial barrier disruption and vascular remodeling. Inhibiting the PKR–ISR axis protects against mitomycin C-induced endothelial damage.
Deng et al. show that endothelial cells respond to high fluid shear stress by KLF2-mediated induction of the BMP–Smad1/5 pathway inhibitor BMPER, resulting in outward vessel remodeling, and apply this knowledge to develop an approach that improves vessel remodeling in mouse models of diabetes.
Using bulk heart transcriptomics of rat models of right and left ventricle failure, Jurida et al. examined transcriptional changes in cardiomyocytes during the progression of heart failure and the overlap with transcriptomics from humans with chronic thromboembolic pulmonary hypertension (CTEPH), identifying more than 50 genes whose expression levels correlate with the severity of right heart disease.
Sakata et al. performed a prospective personalized mechanistic computational (digital twin) study focused on characterizing the arrhythmogenic properties of the atrial fibrotic substrate in patients with persistent atrial fibrillation, and they introduce here a novel mechanism-oriented strategy for optimal ablation.
Bergstedt et al. show that the effects of genetic liability to major depressive disorder can cause an increase in cardiovascular risk and that metabolic, psychological and lifestyle factors are partly responsible for this association.
Zhang et al. show that Egr1 regulates transient senescence during neonatal heart regeneration and upon agrin-mediated cardiac repair in adult mice, acting downstream of the integrin–FAK–ERK–Akt1 axis in cardiac fibroblasts.
Eberhard et al. show that SEMA3A regulates liver sinusoidal endothelial cell fenestrations by signaling through NRP1 and LIMK1, revealing a pathway that connects hyperlipidemia to the development of steatotic liver disease.
Lambert, Oc et al. reconstruct gene regulatory networks from single-cell transcriptomics and epigenetic profiling, compare mouse and human data, and report previously unrecognized regulators of vascular smooth muscle cell proliferation in disease.
Amoedo-Leite et al. report that, in ischemic tissue, a subset of macrophages adopts mural cell-like morphology, gene expression and function, which is crucial for injury healing.
Htet et al. identify and characterize a transcriptional enhancer that regulates cardiomyocyte maturation and function in human pluripotent stem cell and mouse models.
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.