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.
Rjoob et al. develop CardioKG, a knowledge graph built on cardiac imaging traits to identify genetic associations and potential therapeutic strategies and drug repurposing opportunities for cardiovascular diseases.
Kathiriya et al. identify a cardiac progenitor lineage with expression of Tbx5 and anterior heart field-specific expression of Mef2c that bisects the intraventricular septum during development and show that alterations in this lineage lead to congenital heart defects in mice.
The 2025 Nobel Prize in Physiology or Medicine honored a scientific breakthrough with hidden cardiovascular potential: regulatory T cells and peripheral immune tolerance. These mechanisms provide a paradigm shift for understanding and treating cardiovascular disease, dampening inflammation without compromising immunity, and offering safer and more effective therapies.
Long COVID is a major global health challenge but the underlying mechanisms are unclear, hampering the development of effective therapies. Evidence points to a causal link between thromboembolic processes and symptom persistence, suggesting a role for vascular and coagulation abnormalities in the pathogenesis of this complex syndrome.
Schuermans et al. discovered that genetic predisposition to thromboembolism is associated with a greater risk of post-acute sequelae after SARS-CoV-2 infection, including long COVID, and downstream analyses implicated PAR-1 as a potential contributor to long COVID.
Giles et al. developed a method for noninvasive absorbance measurement of mitochondrial hemes to monitor the mitochondrial membrane potential in the perfused heart. They then applied this approach to show how the mitochondrial membrane potential changed during cardiac ischemia.
Patsy et al. review the relationship between the heart and the nervous system during development and the functional consequences of cardiac innervation. They describe the generation of cardiomyocytes and autonomic neurons and propose a roadmap toward the development of cardiac innervation models.
There is great interest in modeling human HFpEF in animals to identify underlying mechanisms and ultimately improve sorely needed therapies. Our current models are a step forward but still fall short in several crucial ways, particularly by not capturing the severity of heart failure features common in patients.
We developed an adeno-associated virus-based, conditional and reversible gene therapy. Using this approach to transiently induce YAP activation in cardiomyocytes either before or after ischemic injury in mice, we could improve cardiac function.
Meng et al. develop the adeno-associated virus 9-based therapy CM-YAPon to transiently and inducibly express YAP in the heart. In mice, CM-YAPon promoted cardiomyocyte cell cycle reentry and reprogrammed the cardiac microenvironment. The CM-YAPon gene therapy improved cardiac function after myocardial infarction (MI) and conferred cardioprotection before MI.
Heart failure and cancer share risk factors and biological pathways, yet their interplay remains underexplored. This Comment calls for coordinated research, precision medicine approaches and policy changes to advance the emerging field of cardio-oncology.
Neo et al. map blood emergence from three hemogenic endothelial (HE) populations biased toward distinct blood fates. HE primed for stem progenitors shows elevated chromatin and RNA splicing gene expression and greater isoform diversity.
Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.
Anthrax toxin receptor 1 (ANTXR1), an integrin-like transmembrane protein, is a docking platform for anthrax toxin and mediates cell–extracellular matrix interactions. New work shows that ANTXR1 stabilizes transforming growth factor-β receptors on cardiac fibroblasts, leading to profibrotic signaling and pathological remodeling of the heart.
