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A new study identifies microRNAs that are enriched in exosomes secreted from cardiosphere-derived cells and which are associated with cardiac repair in pigs and humans with dilated cardiomyopathy.
A new study identifies the mitochondrial protein ALDH4A1 as a potential biomarker of atherosclerosis and as a target antigen of protective autoantibody A12, which might have therapeutic potential.
In the AFFIRM-AHF trial, the use of intravenous ferric carboxymaltose in patients with acute heart failure and iron deficiency was associated with a reduction in hospitalization for heart failure and cardiovascular death.
In patients with recurrent pericarditis, treatment with rilonacept, an engineered fusion protein that acts as an IL-1 trap, leads to a rapid resolution of recurrent pericarditis episodes and reduces the risk of pericarditis recurrence.
Omecamtiv mecarbil (a myosin activator) and mavacamten (a myosin inhibitor) have beneficial effects in patients with heart failure with reduced ejection fraction or obstructive hypertrophic cardiomyopathy, respectively.
Findings from two clinical trials indicate that cryoablation as first-line treatment is superior to drug therapy for the prevention of atrial arrhythmia recurrence in patients with paroxysmal atrial fibrillation.
In the TIPS-3 trial, a single polypill comprising blood-pressure-lowering and cholesterol-lowering drugs, together with a daily dose of aspirin, reduced cardiovascular events in people at risk of cardiovascular disease.
Sotagliflozin reduces the risk of adverse cardiovascular events in patients with type 2 diabetes mellitus and chronic kidney disease or worsening heart failure according to the SCORED and SOLOIST-WHF trials.
In patients with heart failure who are carriers of a clonal haematopoiesis driver mutation in DNMT3A, circulating monocytes have a pro-inflammatory transcriptome, which might worsen disease progression.
A new study identifies a previously unknown paracrine signalling system in the human atrium that is mediated by calcitonin produced by atrial cardiomyocytes and is involved in controlling atrial fibrogenesis and arrhythmia.
A metabolomics approach to assess heart energy metabolism in humans provides new insights into what fuels are used by both the failing and non-failing heart.
After myocardial infarction in mice, cardiac macrophages produce matrix metalloproteinase 14, which promotes endothelial-to-mesenchymal transition, cardiac fibrosis and myocardial dysfunction.
A new study shows that crosstalk between the ERBB2 and Hippo–YAP pathways is required for robust cardiac regeneration after myocardial infarction. ERBB2–ERK–YAP mechanotransduction signalling and epithelial–mesenchymal transition-like processes in cardiomyocytes can trigger regeneration even after functional deterioration and scarring.
A newly identified mechanism of piRNA-mediated post-transcriptional regulation of gene expression is associated with pathological hypertrophy, cardiac remodelling and heart failure.
Higher levels of angiotensin-converting enzyme 2 in plasma are associated with a greater risk of major cardiovascular disease events, according to a global, population-based study.
A new single-cell data set defines the immune response to myocardial infarction, from origins in the bone marrow and its translational potential in the blood to diversification and regulation within the heart.
The cellular composition of the heart is highly heterogeneous, plastic and sex-specific. These findings have important implications for understanding the functional specialization of the heart and also highlight the importance of considering biological sex in preclinical studies.
A new study shows that exosomes secreted by cardiac cells derived from human induced pluripotent stem cells improve myocardial recovery without arrhythmogenic complications and might provide an acellular therapeutic option for myocardial infarction.
A network of macrophages in the heart supports cardiac health and function by removing dysfunctional mitochondria and waste material released from cardiomyocytes in subcellular particles called exophers.
A study in an in vitro model of RBM20-deficient dilated cardiomyopathy suggests that pharmacological upregulation of RBM20 with all-trans retinoic acid is a potential therapeutic strategy in patients with a heterozygous RBM20 mutation.
