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Barrachina et al. show that the uptake of fatty acids by the scavenger receptor CD36 and phospholipid remodeling are essential for megakaryocyte maturation and platelet production.
The US Food and Drug Administration (FDA) has approved sotagliflozin with a broad heart-failure indication, even in the absence of trial data in patients without diabetes. No one knows what the benefits or risks of inhibiting SGLT1 in the heart might be.
Several experimental systems have been used over the past five decades to address important questions in cardiac development and congenital heart disease. Here we discuss the strengths and limitations of available models, and how the use of different models synergistically is needed for a deeper understanding of these complex diseases.
Patients with chronic ischemic heart disease — an important cause of heart failure — show altered myocardial bioenergetics with metabolomic and transcriptomic changes that seem to occur at a global, rather than regional, level in human hearts.
Wang, Brady, et al. review the current knowledge on how ECM mechanics regulate vascular homeostasis and dysfunction and the approaches available to examine ECM mechanisms at tissue and cellular levels and to model pathological cell–ECM mechanical interactions for therapeutic applications.
A single-center, observational cohort study assessing the mitochondrial bioenergetics of left ventricular tissue from patients undergoing coronary artery bypass grafting surgery suggests that viable myocardium has global alterations in bioenergetics and transcriptome without large regional differences between areas with or without inducible ischemia.
Barrachina et al. present an extensive lipidomic analysis at different stages of thrombopoiesis and, through in vitro and in vivo experiments, demonstrate that fatty acid uptake, largely dependent on the scavenger receptor CD36, and its regulation are essential for megakaryocyte maturation and platelet production.
Han, Fang et al. show that the deubiquitinase JOSD2 deubiquitinates and stabilizes SERCA2a in cardiomyocytes, which results in normalized calcium handling and reduced cardiac pathology under hypertensive stress.
Lin et al. show that MCM8 protects vascular health by mediating nitric-oxide-dependent mitophagy. The common East-Asian MCM8-P276 variant is ineffective in mitophagy, which potentiates cGAS-STING and type I interferon signaling in a mouse model of Kawasaki disease.